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1

Hyperglycemia, glucose intolerance, hypertension and socioeconomic position in eastern Nepal.  

PubMed

Abstract. The present study was undertaken to evaluate differences between urban and rural Nepali populations in terms of hyperglycemia, socioeconomic position (SEP) and hypertension, through a community based survey in Sunsari District, eastern Nepal. Blood glucose levels were measured in participants (N = 2,006) S30 years old from urban and rural communities and were classified according to WHO criteria (1998) into normoglycemia (NGY), impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and hyperglycemia (HGY). SEP was assessed by structured health interview along with anthropometric measurements and behavioral variables. Hypertension was classified per Joint National Committee (JNC-VII) criteria. Ten point three percent and 11.9% of subjects in this survey (13.3% urban and 11.0% rural) gave a family history and personal history of diabetes mellitus, respectively. Of urban participants (n = 736) with no history of diabetes 70 (9.5%) had HGY and 143 (19.4%) had glucose intolerance (IFG and IGT). Of rural participants (n = 1,270) 114 (9.0%) had HGY and 176 (13.9%) had glucose intolerance. There was an increasing trend in numbers of cases of hyperglycemia and intolerance with increasing age (chi2 198.2, p < 0.001), body mass index (BMI) (chi2 35.1, p < 0.001), SEP (chi2 48.5, p < 0.001) and hypertension (chi2 130.6, p < 0.001). Rural participants had a lower odds ratio [0.706; 95% confidence interval (CI) 0.455-1.096] of having hyperglycemia than urban participants. Individuals with medium and higher SEP had a lower odds ratio (0.878; CI 0.543-1.868) and higher odds ratio (1.405; CI 0.798-2.474), respectively, compared to individuals with lower SEP of having HGY. Both urban and rural populations are at risk for hyperglycemia and glucose intolerance. Individuals having a medium SEP had lower risk of diabetes mellitus than individuals from lower and higher SEP. PMID:21323183

Mehta, K D; Karki, P; Lamsal, M; Paudel, I S; Majhi, S; Das, B K L; Sharma, S; Jha, N; Baral, N

2011-01-01

2

Comparison between valsartan and amlodipine regarding cardiovascular morbidity and mortality in hypertensive patients with glucose intolerance: NAGOYA HEART Study.  

PubMed

It has not been fully examined whether angiotensin II receptor blocker is superior to calcium channel blocker to reduce cardiovascular events in hypertensive patients with glucose intolerance. A prospective, open-labeled, randomized, controlled trial was conducted for Japanese hypertensive patients with type 2 diabetes mellitus or impaired glucose tolerance. A total of 1150 patients (women: 34%; mean age: 63 years; diabetes mellitus: 82%) were randomly assigned to receive either valsartan- or amlodipine-based antihypertensive treatment. Primary outcome was a composite of acute myocardial infarction, stroke, coronary revascularization, admission attributed to heart failure, or sudden cardiac death. Blood pressure was 145/82 and 144/81 mm Hg, and glycosylated hemoglobin was 7.0% and 6.9% at baseline in the valsartan group and the amlodipine group, respectively. Both of them were equally controlled between the 2 groups during the study. The median follow-up period was 3.2 years, and primary outcome had occurred in 54 patients in the valsartan group and 56 in the amlodipine group (hazard ratio: 0.97 [95% CI: 0.66-1.40]; P=0.85). Patients in the valsartan group had a significantly lower incidence of heart failure than in the amlodipine group (hazard ratio: 0.20 [95% CI: 0.06-0.69]; P=0.01). Other components and all-cause mortality were not significantly different between the 2 groups. Composite cardiovascular outcomes were comparable between the valsartan- and amlodipine-based treatments in Japanese hypertensive patients with glucose intolerance. Admission because of heart failure was significantly less in the valsartan group. PMID:22232134

Muramatsu, Takashi; Matsushita, Kunihiro; Yamashita, Kentaro; Kondo, Takahisa; Maeda, Kengo; Shintani, Satoshi; Ichimiya, Satoshi; Ohno, Miyoshi; Sone, Takahito; Ikeda, Nobuo; Watarai, Masato; Murohara, Toyoaki

2012-03-01

3

Relationship of the angiotensin-converting enzyme gene polymorphism to glucose intolerance, insulin resistance, and hypertension in NIDDM.  

PubMed

The deletion (D) allele of the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been shown to be associated with cardiovascular and renal diseases in diabetes mellitus, but the mechanism underlying this association is not known. In addition, recent studies of the effect of the ACE gene on blood pressure have yielded conflicting results. Therefore, we studied the association of the ACE gene I/D polymorphism with glucose intolerance and insulin resistance, and the contribution of this locus to genetic susceptibility to hypertension in non-insulin-dependent diabetic mellitus (NIDDM). We analysed the ACE genotype in 84 unrelated NIDDM patients with a known disease duration of less than 1 year and in 115 age- and sex-matched controls. The I/D polymorphism was determined by the polymerase chain reaction. There were no differences in ACE genotype distribution and allele frequencies between patients with NIDDM and nondiabetic controls. The frequencies of the D and I alleles in both groups were identical, viz., 0.65 and 0.35, respectively. The NIDDM patients with the DD genotype had significantly higher blood glucose levels in the oral glucose tolerance test than those with the other genotypes; the incremental glucose area under the curve in the order of II, ID, and DD was 7.2+/-2.4, 9.2+/-4.0, and 10.7+/-2.7 mmol/l x h (II vs ID vs DD, P=0.0066 by ANOVA). No significant difference was found between the ACE genotype and serum insulin values. Similarly, there were no differences in body mass index, blood pressure, or serum lipids between the three genotypes. Among the non-diabetic controls, there was no statistically significant association of the I/D polymorphism with serum lipids, blood glucose levels, serum insulin concentrations, or blood pressure values. In conclusion, NIDDM patients with the DD genotype have higher blood glucose levels and are more glucose intolerant; this may help to explain the reported association between the D allele and vascular complications in NIDDM. PMID:9544854

Huang, X H; Rantalaiho, V; Wirta, O; Pasternack, A; Koivula, T; Hiltunen, T; Nikkari, T; Lehtimäki, T

1998-03-01

4

Fatty acid nitroalkenes ameliorate glucose intolerance and pulmonary hypertension in high-fat diet-induced obesity  

PubMed Central

Aims Obesity is a risk factor for diabetes and cardiovascular diseases, with the incidence of these disorders becoming epidemic. Pathogenic responses to obesity have been ascribed to adipose tissue (AT) dysfunction that promotes bioactive mediator secretion from visceral AT and the initiation of pro-inflammatory events that induce oxidative stress and tissue dysfunction. Current understanding supports that suppressing pro-inflammatory and oxidative events promotes improved metabolic and cardiovascular function. In this regard, electrophilic nitro-fatty acids display pleiotropic anti-inflammatory signalling actions. Methods and results It was hypothesized that high-fat diet (HFD)-induced inflammatory and metabolic responses, manifested by loss of glucose tolerance and vascular dysfunction, would be attenuated by systemic administration of nitrooctadecenoic acid (OA-NO2). Male C57BL/6j mice subjected to a HFD for 20 weeks displayed increased adiposity, fasting glucose, and insulin levels, which led to glucose intolerance and pulmonary hypertension, characterized by increased right ventricular (RV) end-systolic pressure (RVESP) and pulmonary vascular resistance (PVR). This was associated with increased lung xanthine oxidoreductase (XO) activity, macrophage infiltration, and enhanced expression of pro-inflammatory cytokines. Left ventricular (LV) end-diastolic pressure remained unaltered, indicating that the HFD produces pulmonary vascular remodelling, rather than LV dysfunction and pulmonary venous hypertension. Administration of OA-NO2 for the final 6.5 weeks of HFD improved glucose tolerance and significantly attenuated HFD-induced RVESP, PVR, RV hypertrophy, lung XO activity, oxidative stress, and pro-inflammatory pulmonary cytokine levels. Conclusions These observations support that the pleiotropic signalling actions of electrophilic fatty acids represent a therapeutic strategy for limiting the complex pathogenic responses instigated by obesity. PMID:24385344

Kelley, Eric E.; Baust, Jeff; Bonacci, Gustavo; Golin-Bisello, Franca; Devlin, Jason E.; St. Croix, Claudette M.; Watkins, Simon C.; Gor, Sonia; Cantu-Medellin, Nadiezhda; Weidert, Eric R.; Frisbee, Jefferson C.; Gladwin, Mark T.; Champion, Hunter C.; Freeman, Bruce A.; Khoo, Nicholas K.H.

2014-01-01

5

Beneficial effects of calcitriol on hypertension, glucose intolerance, impairment of endothelium-dependent vascular relaxation, and visceral adiposity in fructose-fed hypertensive rats.  

PubMed

Besides regulating calcium homeostasis, the effects of vitamin D on vascular tone and metabolic disturbances remain scarce in the literature despite an increase intake with high-fructose corn syrup worldwide. We investigated the effects of calcitriol, an active form of vitamin D, on vascular relaxation, glucose tolerance, and visceral fat pads in fructose-fed rats. Male Wistar-Kyoto rats were divided into 4 groups (n = 6 per group). Group Con: standard chow diet for 8 weeks; Group Fru: high-fructose diet (60% fructose) for 8 weeks; Group Fru-HVD: high-fructose diet as Group Fru, high-dose calcitriol treatment (20 ng / 100 g body weight per day) 4 weeks after the beginning of fructose feeding; and Group Fru-LVD: high-fructose diet as Group Fru, low-dose calcitriol treatment (10 ng / 100 g body weight per day) 4 weeks after the beginning of fructose feeding. Systolic blood pressure was measured twice a week by the tail-cuff method. Blood was examined for serum ionized calcium, phosphate, creatinine, glucose, triglycerides, and total cholesterol. Intra-peritoneal glucose intolerance test, aortic vascular reactivity, the weight of visceral fat pads, adipose size, and adipose angiotensin II levels were analyzed at the end of the study. The results showed that the fructose-fed rats significantly developed hypertension, impaired glucose tolerance, heavier weight and larger adipose size of visceral fat pads, and raised adipose angiotensin II expressions compared with the control rats. High- and low-dose calcitriol reduced modestly systolic blood pressure, increased endothelium-dependent aortic relaxation, ameliorated glucose intolerance, reduced the weight and adipose size of visceral fat pads, and lowered adipose angiotensin II expressions in the fructose-fed rats. However, high-dose calcitriol treatment mildly increased serum ionized calcium levels (1.44 ± 0.05 mmol/L). These results suggest a protective role of calcitriol treatment on endothelial function, glucose tolerance, and visceral adiposity in fructose-fed rats. PMID:25774877

Chou, Chu-Lin; Pang, Cheng-Yoong; Lee, Tony J F; Fang, Te-Chao

2015-01-01

6

Beneficial Effects of Calcitriol on Hypertension, Glucose Intolerance, Impairment of Endothelium-Dependent Vascular Relaxation, and Visceral Adiposity in Fructose-Fed Hypertensive Rats  

PubMed Central

Besides regulating calcium homeostasis, the effects of vitamin D on vascular tone and metabolic disturbances remain scarce in the literature despite an increase intake with high-fructose corn syrup worldwide. We investigated the effects of calcitriol, an active form of vitamin D, on vascular relaxation, glucose tolerance, and visceral fat pads in fructose-fed rats. Male Wistar-Kyoto rats were divided into 4 groups (n = 6 per group). Group Con: standard chow diet for 8 weeks; Group Fru: high-fructose diet (60% fructose) for 8 weeks; Group Fru-HVD: high-fructose diet as Group Fru, high-dose calcitriol treatment (20 ng / 100 g body weight per day) 4 weeks after the beginning of fructose feeding; and Group Fru-LVD: high-fructose diet as Group Fru, low-dose calcitriol treatment (10 ng / 100 g body weight per day) 4 weeks after the beginning of fructose feeding. Systolic blood pressure was measured twice a week by the tail-cuff method. Blood was examined for serum ionized calcium, phosphate, creatinine, glucose, triglycerides, and total cholesterol. Intra-peritoneal glucose intolerance test, aortic vascular reactivity, the weight of visceral fat pads, adipose size, and adipose angiotensin II levels were analyzed at the end of the study. The results showed that the fructose-fed rats significantly developed hypertension, impaired glucose tolerance, heavier weight and larger adipose size of visceral fat pads, and raised adipose angiotensin II expressions compared with the control rats. High- and low-dose calcitriol reduced modestly systolic blood pressure, increased endothelium-dependent aortic relaxation, ameliorated glucose intolerance, reduced the weight and adipose size of visceral fat pads, and lowered adipose angiotensin II expressions in the fructose-fed rats. However, high-dose calcitriol treatment mildly increased serum ionized calcium levels (1.44 ± 0.05 mmol/L). These results suggest a protective role of calcitriol treatment on endothelial function, glucose tolerance, and visceral adiposity in fructose-fed rats. PMID:25774877

Chou, Chu-Lin; Pang, Cheng-Yoong; Lee, Tony J. F.; Fang, Te-Chao

2015-01-01

7

Hypoxia Causes Glucose Intolerance in Humans  

Microsoft Academic Search

Hypoxic respiratory diseases are frequently accompanied by glucose intolerance. We examined whether hypoxia is a cause of glucose intolerance in healthy subjects. In a double-blind within-subject crossover design, hypoxic versus normoxic conditions were induced in 14 healthy men for 30 minutes by decreasing oxygen saturation to 75% (versus 96% in control subjects) under the conditions of a euglycemic clamp. The

Kerstin M. Oltmanns; Hartmut Gehring; Sebastian Rudolf; Bernd Schultes; Stefanie Rook; Ulrich Schweiger; Jan Born; Horst L. Fehm; Achim Peters

2004-01-01

8

Blood Pressure Is Reduced and Insulin Sensitivity Increased in Glucose-Intolerant, Hypertensive Subjects after 15 Days of Consuming High-Polyphenol Dark Chocolate1-3  

Microsoft Academic Search

Flavanols from chocolate appear to increase nitric oxide bioavailability, protect vascular endothelium, and decrease cardiovascular disease (CVD) risk factors. We sought to test the effect of flavanol-rich dark chocolate (FRDC) on endothelial function, insulin sensitivity, b-cell function, and blood pressure (BP) in hypertensive patients with impaired glucose tolerance (IGT). After a run-in phase, 19 hypertensives with IGT (11 males, 8

Davide Grassi; Giovambattista Desideri; Stefano Necozione; Cristina Lippi; Raffaele Casale; Giuliana Properzi; Jeffrey B. Blumberg; Claudio Ferri

9

Sox9-Haploinsufficiency Causes Glucose Intolerance in Claire L. Dubois.  

E-print Network

) investigate whether reduced Sox9 gene dosage leads to impaired glucose homeostasis in adult mice. Employing during adulthood are necessary for normal glucose homeostasis. During development, endocrine and exocrineSox9-Haploinsufficiency Causes Glucose Intolerance in Mice Claire L. Dubois. , Hung Ping Shih

Sander, Maike

10

High iron level in early pregnancy increased glucose intolerance.  

PubMed

High iron stores in pregnancy are essential in preventing negative outcomes for both infants and mothers; however the risk of gestational diabetes mellitus (GDM) might also be increased. We intend to study the relationship between increased iron stores in early pregnancy and the risk of glucose intolerance and GDM. This prospective, observational, single-hospital study involved 104 non-anemic pregnant women, divided into 4 groups based on the quartile values for ferritin at the first trimester of pregnancy. All participants were screened for GDM with 75-g oral glucose tolerance test (OGTT) at 24-28 weeks' gestation. We observed that ferritin levels at early pregnancy were significantly correlated to glucose level after OGTT at 1-h and 2-h (rho=0.21, p<0.05; rho=0.43, p<0.001 respectively). Furthermore, in the higher quartile for ferritin (>38.8?g/L) glycemia at 2-h OGTT was significantly higher than in the others quartiles (p=0.002). In multivariate regression analysis, serum ferritin was a significant determinant of glycemia at 2-h OGTT. Although we did not find a significant association in the incidence of GDM in women with higher serum ferritin levels, probably in reason to the limit power of our study, our data demonstrated that the role of iron excess is tightly involved in the pathogenesis of glucose intolerance. We report for the first time that high ferritin values in early pregnancy are predictors of impaired glucose tolerance in non-anemic women. Individual iron supplementation should be evaluated in order to minimize glucose impairment risk in women with high risk of diabetes. PMID:25441227

Zein, Salam; Rachidi, Samar; Awada, Sanaa; Osman, Mireille; Al-Hajje, Amal; Shami, Nadine; Sharara, Iman; Cheikh-Ali, Khawla; Salameh, Pascale; Hininger-Favier, Isabelle

2015-04-01

11

Effect of macronutrient intake on the development of glucose intolerance during pregnancy1-3  

Microsoft Academic Search

Background: Dietary intake influences glucose tolerance status, yet the relation between macronutrient intake and the development of glucose intolerance during pregnancy has not been adequately ex- amined. Objective: We examined the relation between macronutrient intake early in pregnancy and the development of glucose intolerance. Design: Data are from 1698 women in the Pregnancy, Infection, and Nutrition Study. Dietary intake during

Tina M Saldana; Anna Maria Siega-Riz; Linda S Adair

12

Artificial sweeteners induce glucose intolerance by altering the gut microbiota.  

PubMed

Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment, and are fully transferrable to germ-free mice upon faecal transplantation of microbiota configurations from NAS-consuming mice, or of microbiota anaerobically incubated in the presence of NAS. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage. PMID:25231862

Suez, Jotham; Korem, Tal; Zeevi, David; Zilberman-Schapira, Gili; Thaiss, Christoph A; Maza, Ori; Israeli, David; Zmora, Niv; Gilad, Shlomit; Weinberger, Adina; Kuperman, Yael; Harmelin, Alon; Kolodkin-Gal, Ilana; Shapiro, Hagit; Halpern, Zamir; Segal, Eran; Elinav, Eran

2014-10-01

13

Vitamin E and Vitamin C supplementation does not prevent glucose intolerance in obese-prone rats  

Technology Transfer Automated Retrieval System (TEKTRAN)

Obesity-induced glucose intolerance affects over 70 million Americans. Elevated oxidative stress is associated with development of glucose intolerance. In this work, we tested the hypothesis that supplementation with the anti-oxidants vitamin E (d-alpha-tocopherol acetate; 0.4 g/kg diet) and vitamin...

14

Exercise protects against glucose intolerance in individuals with a small body size at birth  

Microsoft Academic Search

Background. Small body size at birth is a risk factor for Type 2 diabetes. We investigated whether regular exercise is related to lower rates of glucose intolerance in individuals with a small body size at birth and whether birth size affects exercise habits in adulthood.Methods. Five hundred subjects aged 65–75 years with data on birth measurements underwent an oral glucose

Johan G Eriksson; Hilkka Ylihärsilä; Tom Forsén; Clive Osmond; David J. P Barker

2004-01-01

15

Insulin improves ?-cell function in glucose-intolerant rat models induced by feeding a high-fat diet  

Microsoft Academic Search

Insulin therapy has been shown to contribute to extended glycemia remission in newly diagnosed patients with type 2 diabetes mellitus. This study investigated the effects of insulin treatment on pancreatic lipid content, and ?-cell apoptosis and proliferation in glucose-intolerant rats to explore the protective role of insulin on ?-cell function. A rat glucose-intolerant model was induced by streptozotocin and a

Hui-qing Li; Bao-ping Wang; Xiu-Ling Deng; Jiao-yue Zhang; Yong-bo Wang; Juan Zheng; Wen-fang Xia; Tian-shu Zeng; Lu-lu Chen

2011-01-01

16

Herbal constituent sequoyitol improves hyperglycemia and glucose intolerance by targeting hepatocytes, adipocytes, and ?-cells  

PubMed Central

The prevalence of insulin resistance and type 2 diabetes increases rapidly; however, treatments are limited. Various herbal extracts have been reported to reduce blood glucose in animals with either genetic or dietary type 2 diabetes; however, plant extracts are extremely complex, and leading compounds remain largely unknown. Here we show that 5-O-methyl-myo-inositol (also called sequoyitol), a herbal constituent, exerts antidiabetic effects in mice. Sequoyitol was chronically administrated into ob/ob mice either orally or subcutaneously. Both oral and subcutaneous administrations of sequoyitol decreased blood glucose, improved glucose intolerance, and enhanced insulin signaling in ob/ob mice. Sequoyitol directly enhanced insulin signaling, including phosphorylation of insulin receptor substrate-1 and Akt, in both HepG2 cells (derived from human hepatocytes) and 3T3-L1 adipocytes. In agreement, sequoyitol increased the ability of insulin to suppress glucose production in primary hepatocytes and to stimulate glucose uptake into primary adipocytes. Furthermore, sequoyitol improved insulin signaling in INS-1 cells (a rat ?-cell line) and protected INS-1 cells from streptozotocin- or H2O2-induced injury. In mice with streptozotocin-induced ?-cell deficiency, sequoyitol treatments increased plasma insulin levels and decreased hyperglycemia and glucose intolerance. These results indicate that sequoyitol, a natural, water-soluble small molecule, ameliorates hyperglycemia and glucose intolerance by increasing both insulin sensitivity and insulin secretion. Sequoyitol appears to directly target hepatocytes, adipocytes, and ?-cells. Therefore, sequoyitol may serve as a new oral diabetes medication. PMID:22297305

Shen, Hong; Shao, Mengle; Cho, Kae Won; Wang, Suqing; Chen, Zheng; Sheng, Liang; Wang, Ting; Liu, Yong

2012-01-01

17

Ozone induces glucose intolerance and systemic metabolic effects in young and aged brown Norway rats?  

PubMed Central

Air pollutants have been associated with increased diabetes in humans. We hypothesized that ozone would impair glucose homeostasis by altering insulin signaling and/or endoplasmic reticular (ER) stress in young and aged rats. One, 4, 12, and 24 month old Brown Norway (BN) rats were exposed to air or ozone, 0.25 or 1.0 ppm, 6 h/day for 2 days (acute) or 2 d/week for 13 weeks (subchronic). Additionally, 4 month old rats were exposed to air or 1.0 ppm ozone, 6 h/day for 1 or 2 days (time-course). Glucose tolerance tests (GTT) were performed immediately after exposure. Serum and tissue biomarkers were analyzed 18 h after final ozone for acute and subchronic studies, and immediately after each day of exposure in the time-course study. Age-related glucose intolerance and increases in metabolic biomarkers were apparent at baseline. Acute ozone caused hyperglycemia and glucose intolerance in rats of all ages. Ozone-induced glucose intolerance was reduced in rats exposed for 13 weeks. Acute, but not subchronic ozone increased ?2-macroglobulin, adiponectin and osteopontin. Time-course analysis indicated glucose intolerance at days 1 and 2 (2> 1), and a recovery 18 h post ozone. Leptin increased day 1 and epinephrine at all times after ozone. Ozone tended to decrease phosphorylated insulin receptor substrate-1 in liver and adipose tissues. ER stress appeared to be the consequence of ozone induced acute metabolic impairment since transcriptional markers of ER stress increased only after 2 days of ozone. In conclusion, acute ozone exposure induces marked systemic metabolic impairments in BN rats of all ages, likely through sympathetic stimulation. PMID:24103449

Bass, V.; Gordon, C.J.; Jarema, K.A.; MacPhail, R.C.; Cascio, W.E.; Phillips, P.M.; Ledbetter, A.D.; Schladweiler, M.C.; Andrews, D.; Miller, D.; Doerfler, D.L.; Kodavanti, U.P.

2015-01-01

18

Ozone induces glucose intolerance and systemic metabolic effects in young and aged brown Norway rats  

SciTech Connect

Air pollutants have been associated with increased diabetes in humans. We hypothesized that ozone would impair glucose homeostasis by altering insulin signaling and/or endoplasmic reticular (ER) stress in young and aged rats. One, 4, 12, and 24 month old Brown Norway (BN) rats were exposed to air or ozone, 0.25 or 1.0 ppm, 6 h/day for 2 days (acute) or 2 d/week for 13 weeks (subchronic). Additionally, 4 month old rats were exposed to air or 1.0 ppm ozone, 6 h/day for 1 or 2 days (time-course). Glucose tolerance tests (GTT) were performed immediately after exposure. Serum and tissue biomarkers were analyzed 18 h after final ozone for acute and subchronic studies, and immediately after each day of exposure in the time-course study. Age-related glucose intolerance and increases in metabolic biomarkers were apparent at baseline. Acute ozone caused hyperglycemia and glucose intolerance in rats of all ages. Ozone-induced glucose intolerance was reduced in rats exposed for 13 weeks. Acute, but not subchronic ozone increased ?{sub 2}-macroglobulin, adiponectin and osteopontin. Time-course analysis indicated glucose intolerance at days 1 and 2 (2 > 1), and a recovery 18 h post ozone. Leptin increased day 1 and epinephrine at all times after ozone. Ozone tended to decrease phosphorylated insulin receptor substrate-1 in liver and adipose tissues. ER stress appeared to be the consequence of ozone induced acute metabolic impairment since transcriptional markers of ER stress increased only after 2 days of ozone. In conclusion, acute ozone exposure induces marked systemic metabolic impairments in BN rats of all ages, likely through sympathetic stimulation. - Highlights: • Air pollutants have been associated with increased diabetes in humans. • Acute ozone exposure produces profound metabolic alterations in rats. • Age influences metabolic risk factors in aging BN rats. • Acute metabolic effects are reversible and repeated exposure reduces these effects. • Ozone metabolic effects are only slightly exacerbated in geriatric rats.

Bass, V. [Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC (United States); Gordon, C.J.; Jarema, K.A.; MacPhail, R.C. [Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC (United States); Cascio, W.E. [Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC (United States); Phillips, P.M. [Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC (United States); Ledbetter, A.D.; Schladweiler, M.C. [Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC (United States); Andrews, D. [Research Cores Unit, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC (United States); Miller, D. [Curriculum in Toxicology, University of North Carolina, Chapel Hill, NC (United States); Doerfler, D.L. [Research Cores Unit, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC (United States); Kodavanti, U.P., E-mail: kodavanti.urmila@epa.gov [Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC (United States)

2013-12-15

19

Muscle Histidine-Containing Dipeptides Are Elevated by Glucose Intolerance in Both Rodents and Men  

PubMed Central

Objective Muscle carnosine and its methylated form anserine are histidine-containing dipeptides. Both dipeptides have the ability to quench reactive carbonyl species and previous studies have shown that endogenous tissue levels are decreased in chronic diseases, such as diabetes. Design and Methods Rodent study: Skeletal muscles of rats and mice were collected from 4 different diet-intervention studies, aiming to induce various degrees of glucose intolerance: 45% high-fat feeding (male rats), 60% high-fat feeding (male rats), cafeteria feeding (male rats), 70% high-fat feeding (female mice). Body weight, glucose-tolerance and muscle histidine-containing dipeptides were assessed. Human study: Muscle biopsies were taken from m. vastus lateralis in 35 males (9 lean, 8 obese, 9 prediabetic and 9 newly diagnosed type 2 diabetic patients) and muscle carnosine and gene expression of muscle fiber type markers were measured. Results Diet interventions in rodents (cafeteria and 70% high-fat feeding) induced increases in body weight, glucose intolerance and levels of histidine-containing dipeptides in muscle. In humans, obese, prediabetic and diabetic men had increased muscle carnosine content compared to the lean (+21% (p>0.1), +30% (p<0.05) and +39% (p<0.05), respectively). The gene expression of fast-oxidative type 2A myosin heavy chain was increased in the prediabetic (1.8-fold, p<0.05) and tended to increase in the diabetic men (1.6-fold, p = 0.07), compared to healthy lean subjects. Conclusion Muscle histidine-containing dipeptides increases with progressive glucose intolerance, in male individuals (cross-sectional). In addition, high-fat diet-induced glucose intolerance was associated with increased muscle histidine-containing dipeptides in female mice (interventional). Increased muscle carnosine content might reflect fiber type composition and/or act as a compensatory mechanism aimed at preventing cell damage in states of impaired glucose tolerance. PMID:25803044

Stegen, Sanne; Everaert, Inge; Deldicque, Louise; Vallova, Silvia; de Courten, Barbora; Ukropcova, Barbara; Ukropec, Jozef; Derave, Wim

2015-01-01

20

Control of obesity and glucose intolerance via building neural stem cells in the hypothalamus?  

PubMed Central

Neural stem cells (NSCs) were recently revealed to exist in the hypothalamus of adult mice. Here, following our observation showing that a partial loss of hypothalamic NSCs caused weight gain and glucose intolerance, we studied if NSCs-based cell therapy could be developed to control these disorders. While hypothalamus-implanted NSCs failed to survive in mice with obesity, NF-?B inhibition induced survival and neurogenesis of these cells, leading to effects in counteracting obesity and glucose intolerance. To generate an alternative cell source, we revealed that iPS-derived NSCs were converted into htNSCs by neuropeptide treatment. Of note, obesity condition potentiated the transfer of carotid artery-injected NSCs into the hypothalamus. These iPS-derived cells when engineered with NF-?B inhibition were also effective in reducing obesity and glucose intolerance, and neurogenesis towards POMCergic and GABAergic lineages was accountable. In conclusion, building NSCs in the hypothalamus represents a strategy for controlling obesity and glucose disorders. PMID:24749061

Li, Juxue; Tang, Yizhe; Purkayastha, Sudarshana; Yan, Jingqi; Cai, Dongsheng

2014-01-01

21

Oral administration of branched chain amino acids improves virus-induced glucose intolerance in mice  

Microsoft Academic Search

We investigated the therapeutic effect of branched chain amino acids (BCAA) on mice with glucose intolerance induced by encephalomyocarditis virus (EMCV). Male DBA\\/2 mice were divided into three groups: treated with BCAA, (such as valine, leucine, and isoleucine), untreated, and control. BCAA-treated and -untreated groups were inoculated intraperitoneally with the NDK25 variant of EMCV at 200 plaque-forming units per mouse.

Toshihiro Utsugi; Akihiro Yoshida; Tsugiyasu Kanda; Isao Kobayashi; Masahiko Kurabayashi; Shoichi Tomono; Shoji Kawazu; Yutaka Tajima; Ryozo Nagai

2000-01-01

22

Retinol-Binding Protein 4 Levels in Obese Children and Adolescents with Glucose Intolerance  

Microsoft Academic Search

Background: Retinol-binding protein 4 (RBP4) is known to be involved in obesity-associated insulin resistance. Aims: To study the relationships between the degree of adiposity, insulin resistance indices, plasma lipids, inflammatory parameters, glucose intolerance (GI) status and plasma RBP4 levels in obese children and adolescents. Patients and Methods: Prospective study comprising 199 obese patients (95 boys) aged 8–16 years (11.8 ±

D. Yeste; J. Vendrell; R. Tomasini; L. L. Gallart; M. Clemente; I. Simón; M. Albisu; M. Gussinyé; L. Audi; A. Carrascosa

2010-01-01

23

Chronic stress aggravates glucose intolerance in leptin receptor-deficient (db/db) mice.  

PubMed

Genetic predisposition and environmental challenges interact to determine individual vulnerability to obesity and type 2 diabetes. We previously established a mouse model of chronic subordination stress-induced hyperphagia, obesity, metabolic like-syndrome and insulin resistance in the presence of a high-fat diet. However, it remains to be established if social stress could also aggravate glucose intolerance in subjects genetically predisposed to develop obesity and type 2 diabetes. To answer this question, we subjected genetically obese mice due to deficiency of the leptin receptor (db/db strain) to chronic subordination stress. Over five weeks, subordination stress in db/db mice led to persistent hyperphagia, hyperglycemia and exacerbated glucose intolerance altogether suggestive of an aggravated disorder when compared to controls. On the contrary, body weight and fat mass were similarly affected in stressed and control mice likely due to the hyperactivity shown by subordinate mice. Stressed db/db mice also showed increased plasma inflammatory markers. Altogether our results suggest that chronic stress can aggravate glucose intolerance but not obesity in genetically predisposed subjects on the basis of a disrupted leptin circuitry. PMID:25791744

Razzoli, Maria; McCallum, Jacob; Gurney, Allison; Engeland, William C; Bartolomucci, Alessandro

2015-05-01

24

Plasma kinetics of an LDL-like nanoemulsion and lipid transfer to HDL in subjects with glucose intolerance  

PubMed Central

OBJECTIVE: Glucose intolerance is frequently associated with an altered plasma lipid profile and increased cardiovascular disease risk. Nonetheless, lipid metabolism is scarcely studied in normolipidemic glucose-intolerant patients. The aim of this study was to investigate whether important lipid metabolic parameters, such as the kinetics of LDL free and esterified cholesterol and the transfer of lipids to HDL, are altered in glucose-intolerant patients with normal plasma lipids. METHODS: Fourteen glucose-intolerant patients and 15 control patients were studied; none of the patients had cardiovascular disease manifestations, and they were paired for age, sex, race and co-morbidities. A nanoemulsion resembling a LDL lipid composition (LDE) labeled with 14C-cholesteryl ester and 3H-free cholesterol was intravenously injected, and blood samples were collected over a 24-h period to determine the fractional clearance rate of the labels by compartmental analysis. The transfer of free and esterified cholesterol, triglycerides and phospholipids from the LDE to HDL was measured by the incubation of the LDE with plasma and radioactivity counting of the supernatant after chemical precipitation of non-HDL fractions. RESULTS: The levels of LDL, non-HDL and HDL cholesterol, triglycerides, apo A1 and apo B were equal in both groups. The 14C-esterified cholesterol fractional clearance rate was not different between glucose-intolerant and control patients, but the 3H-free- cholesterol fractional clearance rate was greater in glucose-intolerant patients than in control patients. The lipid transfer to HDL was equal in both groups. CONCLUSION: In these glucose-intolerant patients with normal plasma lipids, a faster removal of LDE free cholesterol was the only lipid metabolic alteration detected in our study. This finding suggests that the dissociation of free cholesterol from lipoprotein particles occurs in normolipidemic glucose intolerance and may participate in atherogenic signaling. PMID:22522760

Bertato, Marina P; Oliveira, Carolina P; Wajchenberg, Bernardo L; Lerario, Antonio C; Maranhão, Raul C

2012-01-01

25

Immunohistochemical morphometry of pancreatic endocrine cells in diabetic, normoglycaemic glucose-intolerant and normal cats.  

PubMed

The anatomical distribution and volume fractions of pancreatic A cells (glucagon), B cells (insulin) and D cells (somatostatin) were evaluated by an immunoperoxidase technique in 6 diabetic cats, 6 normoglycaemic glucose-intolerant cats and 6 normal control cats. Islets lacking A cells were observed in some sections from the right lobe of the pancreas which correlated with a significantly lower A cell volume fraction in the right pancreatic lobe. Endocrine cell volume fractions in normoglycaemic glucose-intolerant cats were not significantly different from controls. Thus, a reduction in B cell volume fraction was not necessary for the occurrence of impaired glucose tolerance in these cats. However, the reduction of B cell volume fraction in the 2 normoglycaemic glucose-intolerant cats with insular amyloidosis may in part explain the more severely impaired glucose tolerance previously observed in these cats. Insular amyloidosis in our feline diabetics, as in human type II diabetics, was associated with a significant decrease in A and B cell volume fractions. In both human type II and feline diabetes mellitus, however, the reduction in B cell mass does not appear sufficient alone to lead to diabetes mellitus. Therefore, amyloid replacement of functional endocrine cells does not appear to be the primary diabetogenic event in feline diabetes mellitus, but may contribute to progression of the condition due to loss of functional B cell reserves. We thus postulate that a B cell defect precedes deposition of islet amyloid and that these amyloid deposits may thus provide an important biochemical clue to specific B cell derangements occurring in adult-onset diabetics. PMID:2874160

O'Brien, T D; Hayden, D W; Johnson, K H; Fletcher, T F

1986-07-01

26

Glucose intolerance and diabetes following antigen-specific insulitis in diabetes-susceptible "humanized" transgenic mice.  

PubMed

The genetic contribution of antigen-presenting molecules and the environmental ignition of an antigen-specific immune attack to pancreatic beta-cells define autoimmune diabetes. We focused here on generating an antigen-specific model of autoimmune diabetes in humanized double-transgenic mice carrying antigen-presenting HLA-DQ8 diabetes-linked haplotype and expressing human autoantigen GAD65 in pancreatic beta-cells using a relatively diabetes-susceptible strain of mice. Double transgenic (DQ8-GAD65) mice and controls were immunized with cDNA encoding human GAD65 in adenoviral vectors and monitored for glucose intolerance and diabetes. Human-GAD65 immunization induced insulitis, glucose intolerance and diabetes in double-transgenic mice, while controls were insulitis free and glucose tolerant. Glucose intolerance 10 weeks post-immunization was followed by diabetes later on in most animals. Destructive insulitis characterized by inflammation and apoptosis correlated with the diabetes outcome. Humoral immune responses to hGAD65 were sustained in mice with diabetes while transient in non-responders. Insulitis was massive in mice with diabetes while mild in non-responders by the end of the study. Our results show for the first time the occurrence of antigen-specific induced insulitis, impaired glucose homeostasis and diabetes after immunization with a clinically relevant, human autoantigen in the context of HLA-DQ8 diabetes-susceptibility transgenes and human GAD65 expression in beta-cells. This animal model will facilitate studies of mechanisms of disease involved in development of autoimmunity to GAD65 in the context of HLA-DQ8. Furthermore, this model would be ideal for testing therapeutic strategies aimed at preventing human beta-cell loss and/or restoring function in the setting of autoimmune diabetes. PMID:20350527

Elagin, Raya B; Jaume, Juan C

2010-04-23

27

Increased A? production prompts the onset of glucose intolerance and insulin resistance.  

PubMed

Type 2 diabetes (T2D) mellitus and Alzheimer's disease (AD) are two prevalent diseases with comparable pathophysiological features and genetic predisposition. Patients with AD are more susceptible to develop T2D. However, the molecular mechanism linking AD and T2D remains elusive. In this study, we have generated a new mouse model to test the hypothesis that AD would prompt the onset of T2D in mice. To test our hypothesis, we crossed Alzheimer APPswe/PS1dE9 (APP/PS1) transgenic mice with mice partially deficient in leptin signaling (db/+). Body weight, plasma glucose, and insulin levels were monitored. Phenotypic characterization of glucose metabolism was performed using glucose and insulin tolerance tests. ?-Cell mass, islet volume, and islet number were analyzed by histomorphometry. APP/PS1 coexpression in mice with intact leptin receptor signaling did not show any metabolic perturbations in glucose metabolism or insulin sensitivity. In contrast, APP/PS1 coexpression in db/+ mice resulted in nonfasting hyperglycemia, hyperinsulinemia, and hypercholesterolemia without changes in body weight. Conversely, fasting blood glucose and cholesterol levels remained unchanged. Coinciding with altered glucose metabolism, APP/PS1 coexpression in db/+ mice resulted in glucose intolerance, insulin resistance, and impaired insulin signaling. In addition, histomorphometric analysis of pancreata revealed augmented ?-cell mass. Taken together, these findings provide experimental evidence to support the notion that aberrant A? production might be a mechanistic link underlying the pathology of insulin resistance and T2D in AD. PMID:22414803

Jiménez-Palomares, Margarita; Ramos-Rodríguez, Juan José; López-Acosta, José Francisco; Pacheco-Herrero, Mar; Lechuga-Sancho, Alfonso M; Perdomo, Germán; García-Alloza, Mónica; Cózar-Castellano, Irene

2012-06-01

28

Delayed effects of proton irradiation in Macaca mulatta. III. Glucose intolerance. Interim report 1964-1983  

SciTech Connect

A group of rhesus monkeys is being studied in a lifetime survey of the delayed effects of proton irradiation. The animals were exposed during the period 1964 - 1969 to single total-body doses of protons covering the spectrum of energies and total doses that might be expected to occur in space during a major solar flare event. This report describes the results of intravenous glucose tolerance test and the insulin response to glucose challenge in 106 irradiated animals, their control group of 42, and 10 younger control animals. The results indicate that the clearance rate of blood glucose is influenced by the age of the animal and by the type and energy of the radiation. Animals receiving greater than 360 rads of proton irradiation of energies above 138 MeV had significantly slower glucose clearance than nonirradiated controls. Seventeen-twenty-year-old controls were less glucose tolerant than 9-11-year-old controls. Animals with normal glucose tolerance showed considerable individual variation in insulin response, while in animals with marked glucose intolerance (clearance rate < 1.0 %/min), low insulin response was a consistent finding.

Salmon, Y.L.; Yochmowitz, M.G.; Wood, D.H.

1984-03-01

29

Endothelial Function in Women with and without a History of Glucose Intolerance in Pregnancy  

PubMed Central

Background/Aims. Gestational diabetes mellitus (GDM) and milder gestational impaired glucose tolerance (GIGT) identify women who are at risk of developing cardiovascular disease. Endothelial dysfunction, as indicated by impaired flow-mediated dilatation (FMD) on brachial artery ultrasound, is an early marker of vascular disease. Thus, we sought to evaluate endothelial function in women with and without recent glucose intolerance in pregnancy. Methods. One-hundred and seventeen women underwent oral glucose tolerance testing (OGTT) in pregnancy, enabling stratification into those with normal gestational glucose tolerance (n = 59) and those with GDM or GIGT (n = 58). 6 years postpartum, they underwent a repeat of OGTT and brachial artery FMD studies, enabling assessment of FMD and 4 secondary vascular measures: FMD after 60 seconds (FMD60), baseline arterial diameter, peak shear rate, and reactive hyperemia. Results. There were no differences between the normal gestational glucose tolerance and GDM/GIGT groups in FMD (mean 8.5 versus 9.3%, P = 0.61), FMD60 (4.1 versus 5.1%, P = 0.33), baseline diameter (3.4 versus 3.4?mm, P = 0.66), peak shear rate (262.6 versus 274.8?s?1, P = 0.32), and reactive hyperemia (576.6 versus 496.7%, P = 0.07). After covariate adjustment, there were still no differences between the groups. Conclusion. Despite their long-term cardiovascular risk, women with glucose intolerance in pregnancy do not display endothelial dysfunction 6 years postpartum. PMID:23819127

Floras, John; Retnakaran, Ravi

2013-01-01

30

Transgenic Mice Overexpressing Renin Exhibit Glucose Intolerance and Diet-Genotype Interactions  

PubMed Central

Numerous animal and clinical investigations have pointed to a potential role of the renin-angiotensin system (RAS) in the development of insulin resistance and diabetes in conditions of expanded fat mass. However, the mechanisms underlying this association remain unclear. We used a transgenic mouse model overexpressing renin in the liver (RenTgMK) to examine the effects of chronic activation of RAS on adiposity and insulin sensitivity. Hepatic overexpression of renin resulted in constitutively elevated plasma angiotensin II (four- to six-fold increase vs. wild-type, WT). Surprisingly, RenTgMK mice developed glucose intolerance despite low levels of adiposity and insulinemia. The transgenics also had lower plasma triglyceride levels. Glucose intolerance in transgenic mice fed a low-fat diet was comparable to that observed in high-fat fed WT mice. These studies demonstrate that overexpression of renin and associated hyperangiotensinemia impair glucose tolerance in a diet-dependent manner and further support a consistent role of RAS in the pathogenesis of diabetes and insulin resistance, independent of changes in fat mass. PMID:23308073

Fletcher, Sarah J.; Kalupahana, Nishan S.; Soltani-Bejnood, Morvarid; Kim, Jung Han; Saxton, Arnold M.; Wasserman, David H.; De Taeye, Bart; Voy, Brynn H.; Quignard-Boulange, Annie; Moustaid-Moussa, Naima

2013-01-01

31

Antidiabetic-drug combination treatment for glucose intolerance in adult female rats treated acutely with olanzapine.  

PubMed

Second generation antipsychotic drugs are routinely used as treatment for psychotic disorders. Many of these compounds, including olanzapine, cause metabolic side-effects such as impaired glucose tolerance and insulin resistance. Individual antidiabetic drugs can help control elevated glucose levels in patients treated with antipsychotics, but the effects of combining antidiabetics, which routinely occurs with Type 2 diabetes mellitus patients, have never been studied. Presently, we compared the effects of the three different antidiabetics metformin (500mg/kg, p.o.), rosiglitazone (30mg/kg, p.o.) and glyburide (10mg/kg, p.o.) on metabolic dysregulation in adult female rats treated acutely with olanzapine. In addition, dual combinations of each of these antidiabetics were compared head-to-head against each other and the individual drugs. The animals received two daily treatments with antidiabetics and were then treated acutely with olanzapine (10mg/kg, i.p.). Fasting glucose and insulin levels were measured, followed by a 2h glucose tolerance test. Olanzapine caused a large and highly significant glucose intolerance compared to vehicle treated rats. Rosiglitazone decreased glucose levels non-significantly, while both metformin and glyburide significantly decreased glucose levels compared to olanzapine-only treated animals. For antidiabetic dual-drug combinations, the rosiglitazone-metformin group showed an unexpected increase in glucose levels compared to all of the single antidiabetic drugs. However, both the metformin-glyburide and rosiglitazone-glyburide groups showed significantly greater reductions in glucose levels following olanzapine than with single drug treatment alone for metformin or rosiglitazone, bringing glucose levels down to values equivalent to vehicle-only treated animals. These findings indicate that further study of antidiabetic dual-drug combinations in patients treated with antipsychotic drugs is warranted. PMID:24140931

Boyda, Heidi N; Procyshyn, Ric M; Asiri, Yahya; Wu, Claire; Wang, Cathy K; Lo, Ryan; Pang, Catherine C Y; Honer, William G; Barr, Alasdair M

2014-01-01

32

Aerobic exercise improves cognition for older adults with glucose intolerance, a risk factor for Alzheimer's disease.  

PubMed

Impaired glucose regulation is a defining characteristic of type 2 diabetes mellitus (T2DM) pathology and has been linked to increased risk of cognitive impairment and dementia. Although the benefits of aerobic exercise for physical health are well-documented, exercise effects on cognition have not been examined for older adults with poor glucose regulation associated with prediabetes and early T2DM. Using a randomized controlled design, twenty-eight adults (57-83 y old) meeting 2-h tolerance test criteria for glucose intolerance completed 6 months of aerobic exercise or stretching, which served as the control. The primary cognitive outcomes included measures of executive function (Trails B, Task Switching, Stroop, Self-ordered Pointing Test, and Verbal Fluency). Other outcomes included memory performance (Story Recall, List Learning), measures of cardiorespiratory fitness obtained via maximal-graded exercise treadmill test, glucose disposal during hyperinsulinemic-euglycemic clamp, body fat, and fasting plasma levels of insulin, cortisol, brain-derived neurotrophic factor, insulin-like growth factor-1, amyloid-? (A?40 and A?42). Six months of aerobic exercise improved executive function (MANCOVA, p=0.04), cardiorespiratory fitness (MANOVA, p=0.03), and insulin sensitivity (p=0.05). Across all subjects, 6-month changes in cardiorespiratory fitness and insulin sensitivity were positively correlated (p=0.01). For A?42, plasma levels tended to decrease for the aerobic group relative to controls (p=0.07). The results of our study using rigorous controlled methodology suggest a cognition-enhancing effect of aerobic exercise for older glucose intolerant adults. Although replication in a larger sample is needed, our findings potentially have important therapeutic implications for a growing number of adults at increased risk of cognitive decline. PMID:20847403

Baker, Laura D; Frank, Laura L; Foster-Schubert, Karen; Green, Pattie S; Wilkinson, Charles W; McTiernan, Anne; Cholerton, Brenna A; Plymate, Stephen R; Fishel, Mark A; Watson, G Stennis; Duncan, Glen E; Mehta, Pankaj D; Craft, Suzanne

2010-01-01

33

Arsenate-induced maternal glucose intolerance and neural tube defects in a mouse model  

SciTech Connect

Background: Epidemiological studies have linked environmental arsenic (As) exposure to increased type 2 diabetes risk. Periconceptional hyperglycemia is a significant risk factor for neural tube defects (NTDs), the second most common structural birth defect. A suspected teratogen, arsenic (As) induces NTDs in laboratory animals. Objectives: We investigated whether maternal glucose homeostasis disruption was responsible for arsenate-induced NTDs in a well-established dosing regimen used in studies of arsenic's teratogenicity in early neurodevelopment. Methods: We evaluated maternal intraperitoneal (IP) exposure to As 9.6 mg/kg (as sodium arsenate) in LM/Bc/Fnn mice for teratogenicity and disruption of maternal plasma glucose and insulin levels. Selected compounds (insulin pellet, sodium selenate (SS), N-acetyl cysteine (NAC), L-methionine (L-Met), N-tert-Butyl-{alpha}-phenylnitrone (PBN)) were investigated for their potential to mitigate arsenate's effects. Results: Arsenate caused significant glucose elevation during an IP glucose tolerance test (IPGTT). Insulin levels were not different between arsenate and control dams before (arsenate, 0.55 ng/dl; control, 0.48 ng/dl) or after glucose challenge (arsenate, 1.09 ng/dl; control, 0.81 ng/dl). HOMA-IR index was higher for arsenate (3.9) vs control (2.5) dams (p = 0.0260). Arsenate caused NTDs (100%, p < 0.0001). Insulin pellet and NAC were the most successful rescue agents, reducing NTD rates to 45% and 35%. Conclusions: IPGTT, insulin assay, and HOMA-IR results suggest a modest failure of glucose stimulated insulin secretion and insulin resistance characteristic of glucose intolerance. Insulin's success in preventing arsenate-induced NTDs provides evidence that these arsenate-induced NTDs are secondary to elevated maternal glucose. The NAC rescue, which did not restore maternal glucose or insulin levels, suggests oxidative disruption plays a role.

Hill, Denise S.; Wlodarczyk, Bogdan J. [Center for Environmental and Genetic Medicine, Institute of Biosciences and Technology, Texas A and M University System Health Science Center, Houston, TX 77030 (United States); Mitchell, Laura E. [Center for Environmental and Genetic Medicine, Institute of Biosciences and Technology, Texas A and M University System Health Science Center, Houston, TX 77030 (United States); Center for Environmental and Rural Health Texas A and M University, College Station, TX 77843 (United States); Finnell, Richard H. [Center for Environmental and Genetic Medicine, Institute of Biosciences and Technology, Texas A and M University System Health Science Center, Houston, TX 77030 (United States); Interdisciplinary Faculty of Toxicology, Texas A and M University, College Station, TX 77843 (United States); Center for Environmental and Rural Health Texas A and M University, College Station, TX 77843 (United States)], E-mail: rfinnell@ibt.tamhsc.edu

2009-08-15

34

Impaired kisspeptin signaling decreases metabolism and promotes glucose intolerance and obesity  

PubMed Central

The neuropeptide kisspeptin regulates reproduction by stimulating gonadotropin-releasing hormone (GnRH) neurons via the kisspeptin receptor KISS1R. In addition to GnRH neurons, KISS1R is expressed in other brain areas and peripheral tissues, which suggests that kisspeptin has additional functions beyond reproduction. Here, we studied the energetic and metabolic phenotype in mice lacking kisspeptin signaling (Kiss1r KO mice). Compared with WT littermates, adult Kiss1r KO females displayed dramatically higher BW, leptin levels, and adiposity, along with strikingly impaired glucose tolerance. Conversely, male Kiss1r KO mice had normal BW and glucose regulation. Surprisingly, despite their obesity, Kiss1r KO females ate less than WT females; however, Kiss1r KO females displayed markedly reduced locomotor activity, respiratory rate, and energy expenditure, which were not due to impaired thyroid hormone secretion. The BW and metabolic phenotype in Kiss1r KO females was not solely reflective of absent gonadal estrogen, as chronically ovariectomized Kiss1r KO females developed obesity, hyperleptinemia, reduced metabolism, and glucose intolerance compared with ovariectomized WT females. Our findings demonstrate that in addition to reproduction, kisspeptin signaling influences BW, energy expenditure, and glucose homeostasis in a sexually dimorphic and partially sex steroid–independent manner; therefore, alterations in kisspeptin signaling might contribute, directly or indirectly, to some facets of human obesity, diabetes, or metabolic dysfunction. PMID:24937427

Tolson, Kristen P.; Garcia, Christian; Yen, Stephanie; Simonds, Stephanie; Stefanidis, Aneta; Lawrence, Alison; Smith, Jeremy T.; Kauffman, Alexander S.

2014-01-01

35

Liraglutide counteracts obesity and glucose intolerance in a mouse model of glucocorticoid-induced metabolic syndrome  

PubMed Central

Background Glucocorticoid excess is commonly associated with diabetogenic effects, including insulin resistance and glucose intolerance. The effects of the long-term glucagon-like peptide 1 receptor agonist treatment on the metabolic syndrome-like conditions are not yet fully elucidated. Thus, we aimed to test whether long-term liraglutide treatment could be effective as a therapy to counteract the metabolic dysfunctions induced by chronic glucocorticoid exposure. Methods Mice were given corticosterone or vehicle via their drinking water for five consecutive weeks. In addition, mice were treated with once-daily injections of either PBS or liraglutide. Results Liraglutide treatment slowed progression towards obesity and ectopic fat deposition in liver that otherwise occurred in corticosterone-treated mice. The drug reduced the increment in serum insulin caused by corticosterone, but did not affect the reduction of insulin sensitivity. Furthermore, liraglutide improved glucose control in mice exposed to corticosterone as evident by a delay in the progression towards post-prandial hyperglycemia and enhanced glucose clearance during a glucose tolerance test. Glucose-stimulated C-peptide levels were higher in those mice that had received liraglutide and corticosterone compared to mice that had been treated with corticosterone alone, indicating a positive role of liraglutide for beta-cell function. Morphometric analysis revealed increased beta- and alpha-cell masses that were associated with more Ki67-positive islet cells in corticosterone-treated mice irrespective of whether they were co-treated with liraglutide or not. Liraglutide had no discernible effect on alpha-cell mass. Conclusion Liraglutide can be beneficial for subjects at risk of developing metabolic complications as a result of glucocorticoid excess. PMID:24423471

2014-01-01

36

Fructose consumption during pregnancy and lactation induces fatty liver and glucose intolerance in rats  

PubMed Central

Nutritional insults during pregnancy and lactation are health risks for mother and offspring. Both fructose and low protein diets are linked to hepatic steatosis and insulin resistance in non-pregnant animals. We hypothesized that dietary fructose or low protein intake during pregnancy may exacerbate the already compromised glucose homeostasis to induce gestational diabetes and fatty liver. Therefore, we investigated and compared the effects of low protein or fructose intake on hepatic steatosis and insulin resistance in unmated controls and pregnant and lactating rats. Sprague-Dawley rats were fed either a control (CT), a 63% fructose (FR) or an 8% protein (LP) diet. Glucose tolerance test at day 17 of the study revealed greater (P < 0.05) blood glucose at 10 (75.6 vs. 64.0 ± 4.8 mg/dl) and 20 (72.4 vs. 58.6 ± 4.0 mg/dl) min after glucose dose and greater area under the curve (4302.3 vs. 3763.4 ± 263.6 mg·dl?1·min?1) for FR-fed dams compared with CT-fed dams. The rats were euthanized at 21 days postpartum. Both the FR- and LP-fed dams had enlarged (P < 0.05) livers (9.3, 7.1 vs. 4.8 ± 0.2 % body weight) and elevated (P < 0.05) liver triacylglycerol (216.0, 130.0 vs. 19.9 ± 12.6 mg/g liver weight) compared with CT-fed dams. FR induced fatty liver and glucose intolerance in pregnant and lactating rats, but not unmated control rats. The data demonstrate a unique physiological status response to diet resulting in the development of gestational diabetes coupled with hepatic steatosis in FR-fed dams, which is more severe than a LP diet. PMID:22935342

Zou, Mi; Arentson, Emily J.; Teegarden, Dorothy; Koser, Stephanie L.; Onyskow, Laurie; Donkin, Shawn S.

2015-01-01

37

Effect of tripamide on glucose tolerance in patients with hypertension  

Microsoft Academic Search

The effects of tripamide and hydrochlorothiazide on blood pressure and glucose tolerance were studied in 20 hypertensive patients, half of whom had type II diabetes mellitus. Each patient underwent intravenous glucose tolerance testing before and after 4 weeks of treatment with tripamide, 10 mg, and, at a separate time, hydrochlorothiazide, 50 mg. Both tripamide and hydrochlorothiazide lowered blood pressure; for

Kenneth A Conrad; Timothy C Fagan; Stanley M Lee; Jarid A Simons

1986-01-01

38

Glucose Intolerance and Lipid Metabolic Adaptations in Response to Intrauterine and Postnatal Calorie Restriction in Male Adult Rats  

PubMed Central

Enhanced de novo lipogenesis (DNL), an adult hepatic adaption, is seen with high carbohydrate or low-fat diets. We hypothesized that ad libitum intake after prenatal calorie restriction will result in adult-onset glucose intolerance and enhanced DNL with modified lipid metabolic gene expression profile. Stable isotopes were used in 15-month-old adult male rat offspring exposed to prenatal (IUGR), pre- and postnatal (IPGR), or postnatal (PNGR) caloric restriction vs. controls (CON). IUGR vs. CON were heavier with hepatomegaly but unchanged visceral white adipose tissue (WAT), glucose intolerant with reduced glucose-stimulated insulin secretion (GSIS), pancreatic ?-cell mass, and total glucose clearance rate but unsuppressed hepatic glucose production. Liver glucose transporter (Glut) 1 and DNL increased with decreased hepatic acetyl-CoA carboxylase (ACC) and fatty acid synthase but increased WAT fatty acid transport protein-1 and peroxisomal proliferator-activated receptor-?, resistin, and visfatin gene expression. In contrast, PNGR and IPGR were lighter, had reduced visceral WAT, and were glucose tolerant with unchanged hepatic glucose production but with increased GSIS, ?-cell mass, glucose clearance rate, and WAT insulin receptor. Hepatic Glut1 and DNL were also increased in lean IPGR and PNGR with increased hepatic ACC, phosphorylated ACC, and pAMPK and reduced WAT fatty acid transport protein-1, peroxisomal proliferator-activated receptor-?, and ACC?. We conclude the following: 1) the heavy, glucose-intolerant and insulin-resistant IUGR adult phenotype is ameliorated by postnatal caloric restriction; 2) increased DNL paralleling hepatic Glut1 is a biomarker of exposure to early caloric restriction rather than the adult metabolic status; 3) hepatic lipid enzyme expression reflects GSIS rather than DNL; and 4) WAT gene expression reflects an obesogenic vs. lean phenotype. PMID:23183174

Thamotharan, Manikkavasagar; Dai, Yun; Lagishetty, Venu; Matveyenko, Aleksey V.; Lee, W. N. Paul

2013-01-01

39

Maternal and perinatal magnesium restriction predisposes rat pups to insulin resistance and glucose intolerance.  

PubMed

According to the fetal programming hypothesis, impaired intrauterine development results in insulin resistance and associated metabolic disturbances. Recently, we reported increased body fat, a forerunner of insulin resistance, in the pups of mineral-restricted rat dams. To identify the causative mineral(s), the effect of magnesium restriction was assessed. Female weanling WNIN rats (n = 21) consumed ad libitum for 9 wk a 70% magnesium-restricted diet or were pair-fed a control (C) diet (n = 7). After 9 wk, they were mated with control males. Control dams and pups were fed the control diet throughout, whereas 7 Mg-restricted dams were switched to the control diet at parturition and their pups weaned onto the control diet (RP). Pups of the remaining 14 restricted dams were weaned onto the control diet (RW) or the Mg-restricted diet (R). All groups had 8 male pups from weaning. Pups were studied on postnatal d 90 and 180. R pups weighed less than C pups at weaning, but both RP and RW pups caught up with controls by d 90. At this time, R pups were neither insulin resistant nor glucose intolerant, but had a higher percentage of body fat and plasma triglycerides and lower lean body and fat-free mass than C pups. These variables were partially corrected in both RP and RW pups. On postnatal d 180, R, RP, and RW pups were insulin resistant and had a lower insulin response to a glucose challenge than C pups; however, glucose tolerance was impaired only in RW pups. Thus, maternal magnesium restriction irreversibly increases body fat and induces insulin resistance in pups by 6 mo of age, whereas additional perinatal Mg deficiency impairs glucose tolerance. PMID:15930437

Venu, Lagishetty; Kishore, Yedla Durga; Raghunath, Manchala

2005-06-01

40

Glucose intolerance and diabetes mellitus in ulcerative colitis: Pathogenetic and therapeutic implications  

PubMed Central

Diabetes mellitus is one of the most frequent co-morbidities of ulcerative colitis patients. The epidemiological association of these diseases suggested a genetic sharing and has challenged gene identification. Diabetes co-morbidity in ulcerative colitis has also relevant clinical and therapeutic implications, with potential clinical impact on the follow up and outcome of patients. These diseases share specific complications, such as neuropathy, hepatic steatosis, osteoporosis and venous thrombosis. It is still unknown whether the coexistence of these diseases may increase their occurrence. Diabetes and hyperglycaemia represent relevant risk factors for postoperative complications and pouch failure in ulcerative colitis. Medical treatment of ulcerative colitis in patients with diabetes mellitus may be particularly challenging. Corticosteroids are the treatment of choice of active ulcerative colitis. Their use may be associated with the onset of glucose intolerance and diabetes, with difficult control of glucose levels and with complications in diabetic patients. Epidemiologic and genetic evidences about diabetes co-morbidity in ulcerative colitis patients and shared complications and treatment of patients with these diseases have been discussed in the present review. PMID:24707133

Maconi, Giovanni; Furfaro, Federica; Sciurti, Roberta; Bezzio, Cristina; Ardizzone, Sandro; de Franchis, Roberto

2014-01-01

41

Should we do an oral glucose tolerance test in hypertensive men with normal fasting blood-glucose?  

Microsoft Academic Search

The objective of this study was to examine, using the new WHO criteria for diabetes mellitus, whether insulin and glucose before and after an oral glucose tolerance test would predict cardiovascular mortality in hypertensive men with normal fasting blood glucose. A standard oral glucose challenge was performed after an overnight fast in 113 hypertensive men with either hypercholesterolaemia or smoking.

S Agewall

2001-01-01

42

Absence of Perilipin 2 Prevents Hepatic Steatosis, Glucose Intolerance and Ceramide Accumulation in Alcohol-Fed Mice  

PubMed Central

Background Perilipin 2 (Plin2) is a lipid droplet protein that has roles in both lipid and glucose homeostasis. An increase in Plin2 in liver is associated with the development of steatosis, glucose intolerance, and ceramide accumulation in alcoholic liver disease. We investigated the role of Plin2 on energy balance and glucose and lipid homeostasis in wildtype and Plin2 knockout (Plin2KO) mice chronically fed a Lieber-DeCarli liquid ethanol or control diet for six weeks. Methods We performed in vivo measurements of energy intake and expenditure; body composition; and glucose tolerance. After sacrifice, liver was dissected for histology and lipid analysis. Results We found that neither genotype nor diet had a significant effect on final weight, body composition, or energy intake between WT and Plin2KO mice fed alcohol or control diets. Additionally, alcohol feeding did not affect oxygen consumption or carbon dioxide production in Plin2KO mice. We performed glucose tolerance testing and observed that alcohol feeding failed to impair glucose tolerance in Plin2KO mice. Most notably, absence of Plin2 prevented hepatic steatosis and ceramide accumulation in alcohol-fed mice. These changes were related to downregulation of genes involved in lipogenesis and triglyceride synthesis. Conclusions Plin2KO mice chronically fed alcohol are protected from hepatic steatosis, glucose intolerance, and hepatic ceramide accumulation, suggesting a critical pathogenic role of Plin2 in experimental alcoholic liver disease. PMID:24831094

Carr, Rotonya M.; Peralta, Giselle; Yin, Xiaoyan; Ahima, Rexford S.

2014-01-01

43

Profilin-1 Haploinsufficiency Protects Against Obesity-Associated Glucose Intolerance and Preserves Adipose Tissue Immune Homeostasis  

PubMed Central

Metabolic inflammation may contribute to the pathogenesis of obesity and its comorbidities, including type 2 diabetes and cardiovascular disease. Previously, we showed that the actin-binding protein profilin-1 (pfn) plays a role in atherogenesis because pfn heterozygote mice (PfnHet) exhibited a significant reduction in atherosclerotic lesion burden and vascular inflammation. In the current study, we tested whether pfn haploinsufficiency would also limit diet-induced adipose tissue inflammation and insulin resistance (IR). First, we found that a high-fat diet (HFD) upregulated pfn expression in epididymal and subcutaneous white adipose tissue (WAT) but not in the liver or muscle of C57BL/6 mice compared with normal chow. Pfn expression in WAT correlated with F4/80, an established marker for mature macrophages. Of note, HFD elevated pfn protein levels in both stromal vascular cells and adipocytes of WAT. We also found that PfnHet were significantly protected from HFD-induced glucose intolerance observed in pfn wild-type mice. With HFD, PfnHet displayed blunted expression of systemic and WAT proinflammatory cytokines and decreased accumulation of adipose tissue macrophages, which were also preferentially biased toward an M2-like phenotype; this correlated with preserved frequency of regulatory T cells. Taken together, the findings indicate that pfn haploinsufficiency protects against diet-induced IR and inflammation by modulating WAT immune homeostasis. PMID:23884883

Romeo, Giulio R.; Pae, Munkyong; Eberlé, Delphine; Lee, Jongsoon; Shoelson, Steven E.

2013-01-01

44

Insulin sensitivity decreases with obesity, and lean cats with low insulin sensitivity are at greatest risk of glucose intolerance with weight gain  

Microsoft Academic Search

This study quantifies the effects of marked weight gain on glucose and insulin metabolism in 16 cats which increased their weight by an average of 44.2% over 10 months.Significantly, the development of feline obesity was accompanied by a 52% decrease in tissue sensitivity to insulin and diminished glucose effectiveness. In addition, glucose intolerance and abnormal insulin response occurred in some

DJ Appleton; JS Rand; GD Sunvold

2001-01-01

45

Enhanced Lipid Oxidation and Maintenance of Muscle Insulin Sensitivity Despite Glucose Intolerance in a Diet-Induced Obesity Mouse Model  

PubMed Central

Background Diet-induced obesity is a rising health concern which can lead to the development of glucose intolerance and muscle insulin resistance and, ultimately, type II diabetes mellitus. This research investigates the associations between glucose intolerance or muscle insulin resistance and tissue specific changes during the progression of diet-induced obesity. Methodology C57BL/6J mice were fed a normal or high-fat diet (HFD; 60% kcal fat) for 3 or 8 weeks. Disease progression was monitored by measurements of body/tissue mass changes, glucose and insulin tolerance tests, and ex vivo glucose uptake in intact muscles. Lipid metabolism was analyzed using metabolic chambers and ex vivo palmitate assays in intact muscles. Skeletal muscle, liver and adipose tissues were analyzed for changes in inflammatory gene expression. Plasma was analyzed for insulin levels and inflammatory proteins. Histological techniques were used on muscle and liver cryosections to assess metabolic and morphological changes. Principal Findings/Conclusions A rapid shift in whole body metabolism towards lipids was observed with HFD. Following 3 weeks of HFD, elevated total lipid oxidation and an oxidative fiber type shift had occurred in the skeletal muscle, which we propose was responsible for delaying intramyocellular lipid accumulation and maintaining muscle’s insulin sensitivity. Glucose intolerance was present after three weeks of HFD and was associated with an enlarged adipose tissue depot, adipose tissue inflammation and excess hepatic lipids, but not hepatic inflammation. Furthermore, HFD did not significantly increase systemic or muscle inflammation after 3 or 8 weeks of HFD suggesting that early diet-induced obesity does not cause inflammation throughout the whole body. Overall these findings indicate skeletal muscle did not contribute to the development of HFD-induced impairments in whole-body glucose tolerance following 3 weeks of HFD. PMID:23951235

Trajcevski, Karin E.; O’Neill, Hayley M.; Wang, David C.; Thomas, Melissa M.; Al-Sajee, Dhuha; Steinberg, Gregory R.; Ceddia, Rolando B.; Hawke, Thomas J.

2013-01-01

46

Improvements in blood pressure, glucose metabolism, and lipoprotein lipids after aerobic exercise plus weight loss in obese, hypertensive middle-aged men  

Microsoft Academic Search

The clustering of metabolic abnormalities often associated with hypertension, including insulin resistance, glucose intolerance, and dyslipidemia, in middle-aged men may be the result of a decrease in cardiovascular fitness (Vo2max) and the accumulation of body fat with aging. This study examines the effects of a 6-month program of aerobic exercise training plus weight loss (AEX + WL) on Vo2max, body

Donald R. Dengel; James M. Hagberg; Richard E. Pratley; Ellen M. Rogus; Andrew P. Goldberg

1998-01-01

47

Mice lacking the p43 mitochondrial T3 receptor become glucose intolerant and insulin resistant during aging.  

PubMed

Thyroid hormones (TH) play an important regulatory role in energy expenditure regulation and are key regulators of mitochondrial activity. We have previously identified a mitochondrial triiodothyronine (T3) receptor (p43) which acts as a mitochondrial transcription factor of the organelle genome, which leads in vitro and in vivo, to a stimulation of mitochondrial biogenesis. Recently, we generated mice carrying a specific p43 invalidation. At 2 months of age, we reported that p43 depletion in mice induced a major defect in insulin secretion both in vivo and in isolated pancreatic islets, and a loss of glucose-stimulated insulin secretion. The present study was designed to determine whether p43 invalidation influences life expectancy and modulates blood glucose and insulin levels as well as glucose tolerance or insulin sensitivity during aging. We report that from 4 months old onwards, mice lacking p43 are leaner than wild-type mice. p43-/- mice also have a moderate reduction of life expectancy compared to wild type. We found no difference in blood glucose levels, excepted at 24 months old where p43-/- mice showed a strong hyperglycemia in fasting conditions compared to controls animals. However, the loss of glucose-stimulated insulin secretion was maintained whatever the age of mice lacking p43. If up to 12 months old, glucose tolerance remained unchanged, beyond this age p43-/- mice became increasingly glucose intolerant. In addition, if up to 12 months old p43 deficient animals were more sensitive to insulin, after this age we observed a loss of this capacity, culminating in 24 months old mice with a decreased sensitivity to the hormone. In conclusion, we demonstrated that during aging the depletion of the mitochondrial T3 receptor p43 in mice progressively induced an increased glycemia in the fasted state, glucose intolerance and an insulin-resistance several features of type-2 diabetes. PMID:24098680

Bertrand, Christelle; Blanchet, Emilie; Pessemesse, Laurence; Annicotte, Jean Sébastien; Feillet-Coudray, Christine; Chabi, Béatrice; Levin, Jonathan; Fajas, Lluis; Cabello, Gérard; Wrutniak-Cabello, Chantal; Casas, François

2013-01-01

48

Mice Lacking the p43 Mitochondrial T3 Receptor Become Glucose Intolerant and Insulin Resistant during Aging  

PubMed Central

Thyroid hormones (TH) play an important regulatory role in energy expenditure regulation and are key regulators of mitochondrial activity. We have previously identified a mitochondrial triiodothyronine (T3) receptor (p43) which acts as a mitochondrial transcription factor of the organelle genome, which leads in vitro and in vivo, to a stimulation of mitochondrial biogenesis. Recently, we generated mice carrying a specific p43 invalidation. At 2 months of age, we reported that p43 depletion in mice induced a major defect in insulin secretion both in vivo and in isolated pancreatic islets, and a loss of glucose-stimulated insulin secretion. The present study was designed to determine whether p43 invalidation influences life expectancy and modulates blood glucose and insulin levels as well as glucose tolerance or insulin sensitivity during aging. We report that from 4 months old onwards, mice lacking p43 are leaner than wild-type mice. p43?/? mice also have a moderate reduction of life expectancy compared to wild type. We found no difference in blood glucose levels, excepted at 24 months old where p43?/? mice showed a strong hyperglycemia in fasting conditions compared to controls animals. However, the loss of glucose-stimulated insulin secretion was maintained whatever the age of mice lacking p43. If up to 12 months old, glucose tolerance remained unchanged, beyond this age p43?/? mice became increasingly glucose intolerant. In addition, if up to 12 months old p43 deficient animals were more sensitive to insulin, after this age we observed a loss of this capacity, culminating in 24 months old mice with a decreased sensitivity to the hormone. In conclusion, we demonstrated that during aging the depletion of the mitochondrial T3 receptor p43 in mice progressively induced an increased glycemia in the fasted state, glucose intolerance and an insulin-resistance several features of type-2 diabetes. PMID:24098680

Bertrand, Christelle; Blanchet, Emilie; Pessemesse, Laurence; Annicotte, Jean Sébastien; Feillet-Coudray, Christine; Chabi, Béatrice; Levin, Jonathan; Fajas, Lluis; Cabello, Gérard; Wrutniak-Cabello, Chantal; Casas, François

2013-01-01

49

Aerobic Exercise Improves Cognition for Older Adults with Glucose Intolerance, A Risk Factor for Alzheimer’s Disease  

PubMed Central

Impaired glucose regulation is a defining characteristic of type 2 diabetes mellitus (T2DM) pathology and has been linked to increased risk of cognitive impairment and dementia. Although the benefits of aerobic exercise for physical health are well-documented, exercise effects on cognition have not been examined for older adults with poor glucose regulation associated with prediabetes and early T2DM. Using a randomized controlled design, twenty-eight adults (57–83 y old) meeting 2-h tolerance test criteria for glucose intolerance completed 6 months of aerobic exercise or stretching, which served as the control. The primary cognitive outcomes included measures of executive function (Trails B, Task Switching, Stroop, Self-ordered Pointing Test, and Verbal Fluency). Other outcomes included memory performance (Story Recall, List Learning), measures of cardiorespiratory fitness obtained via maximal-graded exercise treadmill test, glucose disposal during hyperinsulinemic-euglycemic clamp, body fat, and fasting plasma levels of insulin, cortisol, brain-derived neurotrophic factor, insulin-like growth factor-1, amyloid-? (A?40 and A?42). Six months of aerobic exercise improved executive function (MANCOVA, p = 0.04), cardiorespiratory fitness (MANOVA, p = 0.03), and insulin sensitivity (p = 0.05). Across all subjects, 6-month changes in cardiorespiratory fitness and insulin sensitivity were positively correlated (p = 0.01). For A?42, plasma levels tended to decrease for the aerobic group relative to controls (p = 0.07). The results of our study using rigorous controlled methodology suggest a cognition-enhancing effect of aerobic exercise for older glucose intolerant adults. Although replication in a larger sample is needed, our findings potentially have important therapeutic implications for a growing number of adults at increased risk of cognitive decline. PMID:20847403

Baker, Laura D.; Frank, Laura L.; Foster-Schubert, Karen; Green, Pattie S; Wilkinson, Charles W.; McTiernan, Anne; Cholerton, Brenna A.; Plymate, Stephen R.; Fishel, Mark A.; Watson, G. Stennis; Duncan, Glen E.; Mehta, Pankaj D.; Craft, Suzanne

2011-01-01

50

The importance of glucose for the freezing tolerance/intolerance of the anuran amphibians Rana catesbeiana and Bufo paracnemis.  

PubMed

Several species of terrestrially hibernating frogs, turtles and insects have developed mechanisms, such as increased plasma glucose, anti-freeze proteins and antioxidant enzymes that resist to freezing, for survival at subzero temperatures. In the present study, we assessed the importance of glucose to cryoresistance of two anuran amphibians: the frog Rana catesbeiana and the toad Bufo paracnemis. Both animals were exposed to -2 degrees C for measurements of plasma glucose levels, liver and muscle glycogen content, haematocrit and red blood cell volume. Frogs survived cold exposure but toads did not. Blood glucose concentration increased from 40.35 +/- 7.25 to 131.87 +/- 20.72 mg/dl (P < 0.01) when the frogs were transferred from 20 to -2 degrees C. Glucose accumulation in response to cold exposition in the frogs was accompanied by a decrease (P < 0.05) in liver glycogen content from 3.94 +/- 0.42 to 1.33 +/- 0.36 mg/100 mg tissue, indicating that liver carbohydrate reserves were probably the primary carbon source of glucose synthesis whereas muscle carbohydrate seems unimportant. In the toads, the cold-induced hyperglycaemia was less (P < 0.05) pronounced (from 27.25 +/- 1.14 to 73.72 +/- 13.50 mg/dl) and no significant change could be measured in liver or muscle glycogen. Cold exposition had no effect on the haematocrit of the frogs but significantly reduced (P < 0.01) the haematocrit of toads from 20.0 +/- 2.1% to 5.8 +/- 1.7% due to a decreased red blood cell volume (from 1532 +/- 63 to 728 +/- 87 mm3). When toads were injected with glucose, blood glucose increased to levels similar to those of frogs and haematocrit did not change, but this failed to make them cryoresistent. In conclusion, the lack of cold-induced glucose catabolism may not be the only mechanism responsible for the freeze intolerance of Bufo paracnemis, a freeze-intolerant species. PMID:10959117

Steiner, A A; Petenusci, S O; Brentegani, L G; Branco, L G

2000-05-01

51

Modification of high saturated fat diet with n-3 polyunsaturated fat improves glucose intolerance and vascular dysfunction  

PubMed Central

Aims The ability of dietary enrichment with monounsaturated (MUFA), n-3, or n-6 polyunsaturated fatty acids (PUFA) to reverse glucose intolerance and vascular dysfunction resulting from excessive dietary saturated fatty acids is not resolved. We hypothesized that partial replacement of dietary saturated fats with n-3 PUFA enriched menhaden oil (MO) would provide greater improvement in glucose tolerance and vascular function compared to n-6 enriched safflower oil (SO) or MUFA-enriched olive oil (OO). Material and Methods We fed mice a high saturated fat diet (60% kcal from lard) for 12 weeks before substituting half the lard with MO, SO or OO for an additional 4 weeks. At the end of 4 weeks, we assessed glucose tolerance, insulin signaling and reactivity of isolated pressurized gracilis arteries. Results After 12 weeks of saturated fat diet, body weights were elevated and glucose tolerance abnormal compared to mice on control diet (13% kcal lard). Diet substituted with MO restored basal glucose levels, glucose tolerance, and indices of insulin signaling (phosphorylated Akt) to normal whereas restoration was limited for SO and OO substitutions. Although dilation to acetylcholine was reduced in arteries from mice on HF, OO and SO diets compared to normal diet, dilation to acetylcholine was fully restored and constriction to phenylephrine reduced in MO fed mice compared to normal. Conclusion We conclude that short term enrichment of an ongoing high fat diet with n-3 PUFA rich MO but not MUFA rich OO or n-6 PUFA rich SO reverses glucose tolerance, insulin signaling, and vascular dysfunction. PMID:22950668

Lamping, KL; Nuno, DW; Coppey, LJ; Holmes, AJ; Hu, S; Oltman, CL; Norris, AW; Yorek, MA

2013-01-01

52

F0 maternal BPA exposure induced glucose intolerance of F2 generation through DNA methylation change in Gck.  

PubMed

BPA, a common environmental endocrine disruptor, has been reported to induce epigenetic changes and disrupt glucose homeostasis in F1 offspring through maternal exposure. However, no studies have examined whether maternal BPA exposure can exert multigenerational effects of glucose metabolic disorder on F2 generation through the altered epigenetic information. The aim of the current study was to investigate whether BPA exposure can disrupt glucose homeostasis in F2 offspring and the underlying epigenetic mechanism. In the present study, F0 pregnant dams were orally administered at a daily dose of 40?g/kg body weight during gestation and lactation. The F1 and F2 generations were obtained and not exposed to BPA anymore. The glucose and insulin tolerance tests were carried out to evaluate the glucose homeostasis level. The relative hormone level and the relative gene expression were also examined. F2 generation was found to exhibited glucose intolerance and insulin resistance in ipGTT and ipITT, as well as the downregulation of glucokinase (Gck) gene in liver. DNA methylation pattern of Gck promoter in the F2 generation of hepatic tissue and F1 generation of sperm was then performed. The Gck promoter in F2 hepatic tissue became completely methylated in the all CpG sites compared with five unmethylated sites in controls. In the F1 sperm, the global DNA methylation was decreased. However, there is only CpG site -314 was differently methylated between BPA and controls in sperm. In conclusion, F0 maternal BPA exposure during gestation and lactation can induce impaired glucose homeostasis in the F2 offspring through the transmission of sperm. The underlying epigenetic modifications in the sperm of F1 generation remain to be further elucidated. PMID:24793715

Li, Gengqi; Chang, Huailong; Xia, Wei; Mao, Zhenxing; Li, Yuanyuan; Xu, Shunqing

2014-08-01

53

Overexpression of Rad in muscle worsens diet-induced insulin resistance and glucose intolerance and lowers plasma triglyceride level  

NASA Astrophysics Data System (ADS)

Rad is a low molecular weight GTPase that is overexpressed in skeletal muscle of some patients with type 2 diabetes mellitus and/or obesity. Overexpression of Rad in adipocytes and muscle cells in culture results in diminished insulin-stimulated glucose uptake. To further elucidate the potential role of Rad in vivo, we have generated transgenic (tg) mice that overexpress Rad in muscle using the muscle creatine kinase (MCK) promoter-enhancer. Rad tg mice have a 6- to 12-fold increase in Rad expression in muscle as compared to wild-type littermates. Rad tg mice grow normally and have normal glucose tolerance and insulin sensitivity, but have reduced plasma triglyceride levels. On a high-fat diet, Rad tg mice develop more severe glucose intolerance than the wild-type mice; this is due to increased insulin resistance in muscle, as exemplified by a rightward shift in the dose-response curve for insulin stimulated 2-deoxyglucose uptake. There is also a unexpected further reduction of the plasma triglyceride levels that is associated with increased levels of lipoprotein lipase in the Rad tg mice. These results demonstrate a potential synergistic interaction between increased expression of Rad and high-fat diet in creation of insulin resistance and altered lipid metabolism present in type 2 diabetes. diabetes mellitus | glucose transport | RGK GTPase | transgenic mouse

Ilany, Jacob; Bilan, Philip J.; Kapur, Sonia; Caldwell, James S.; Patti, Mary-Elizabeth; Marette, Andre; Kahn, C. Ronald

2006-03-01

54

Anoxia tolerance in rice seedlings: exogenous glucose improves growth of an anoxia-'intolerant', but not of a 'tolerant' genotype.  

PubMed

This study demonstrated that, in rice seedlings, genotypic difference in tolerance to anoxia only occurred when anoxia was imposed at imbibition, but not at 3 d after imbibition. When seeds were imbibed and grown in anoxia, IR22 (anoxia-'intolerant') grew much slower and had lower soluble sugar concentrations in coleoptiles and seeds than Amaroo (anoxia-'tolerant'), while Calrose was intermediate. After 3 d in anoxia, the sugar concentrations in embryos and endosperms of anoxic seedlings were nearly 4-fold lower in IR22 than in Amaroo. Sugar deficit in the embryo of IR22 is presumably due to the limitation of sugar mobilization rather than the capacity of transport as shown by similar sugar accumulation ratios of 1.8 between embryo and endosperm in IR22 and Amaroo at 3 d in anoxia. With 20 mol m-3 exogenous glucose, coleoptile extension and fresh weight increments in anoxic seedlings of IR22 were much closer to those in the two other genotypes, nevertheless protein concentration remained lowest on a fresh weight basis in the coleoptiles of IR22; indicating that protein synthesis has a lower priority for energy apportionment during anoxia than processes crucial to coleoptile extension. In contrast to these responses to anoxia imposed at imbibition, IR22 had nearly the same high tolerance to anoxia as Calrose and Amaroo, when anoxia was imposed on seedlings subsequent to 48 h aeration followed by 16 h hypoxic pretreatment. In fact, coleoptiles of anoxic IR22 had higher sugar concentrations and grew faster than Calrose, and exogenous glucose had no effect on the coleoptile extension of IR22. Excised coleoptile tips of IR22 and Amaroo with exogenous glucose had similar rates of ethanol production and were equally tolerant to anoxia. In conclusion, much of the anoxia 'intolerance' of IR22 when germinated in anoxia could be attributed to limited substrate availability to the embryo and coleoptile, presumably due to slow starch hydrolysis in the endosperm. PMID:14504303

Huang, Shaobai; Greenway, Hank; Colmer, Timothy D

2003-10-01

55

Dysregulation of the insulin/IGF binding protein-1 axis in transgenic mice is associated with hyperinsulinemia and glucose intolerance.  

PubMed

The insulin/IGF binding protein-1 (IGFBP-1) axis is important in coordinating insulin- and IGF-mediated regulation of glucose metabolism and glycemia. Dysregulation of the axis may play a role in the pathophysiology of disorders of insulin deficiency and resistance. We have investigated this hypothesis by generating transgenic mice that overexpress hIGFBP-1. To study the axis in its true physiological context, we used a human (h) IGFBP-1 cosmid clone so that transgene expression is responsive to normal hormonal stimuli. hIGFBP-1 mRNA is expressed in a tissue-specific fashion, and measurement of serum protein levels by specific immunoassay indicates normal physiological regulation in response to fasting/feeding and appropriate post-translational modification as indicated by the detection of phosphorylated and nonphosphorylated isoforms of the protein. The hypoglycemic response to exogenous IGF-I is attenuated in transgenic mice. Transgenic mice exhibit an enhanced insulin secretory response to a glucose challenge, although basal and stimulated blood glucose levels are similar to controls. There is a sexual dimorphism in phenotypic expression: male transgenic mice had higher stimulated glucose and insulin levels than did females. Transgenic mice exhibit fasting hyperglycemia and hyperinsulinemia and glucose intolerance in later life, indicating an age-related decline in glucocompetence. These findings demonstrate the importance of the normal inverse relationship between serum insulin and IGFBP-1 levels in glucoregulation and that sustained dysregulation of the insulin/IGF-I/IGFBP-1 axis is associated with impaired glucose tolerance and abnormalities of insulin action. PMID:10868969

Crossey, P A; Jones, J S; Miell, J P

2000-03-01

56

Lifelong Obesity in a Polygenic Mouse Model Prevents Age- and Diet-Induced Glucose Intolerance– Obesity Is No Road to Late-Onset Diabetes in Mice  

PubMed Central

Aims/Hypothesis Visceral obesity holds a central position in the concept of the metabolic syndrome characterized by glucose intolerance in humans. However, until now it is unclear if obesity by itself is responsible for the development of glucose intolerance. Methods We have used a novel polygenic mouse model characterized by genetically fixed obesity (DU6) and addressed age- and high fat diet-dependent glucose tolerance. Results Phenotype selection over 146 generations increased body weight by about 2.7-fold in male 12-week DU6 mice (P<0.0001) if compared to unselected controls (Fzt:DU). Absolute epididymal fat mass was particularly responsive to weight selection and increased by more than 5-fold (P<0.0001) in male DU6 mice. At an age of 6 weeks DU6 mice consumed about twice as much food if compared to unselected controls (P<0.001). Absolute food consumption was higher at all time points measured in DU6 mice than in Fzt:DU mice. Between 6 and 12 weeks of age, absolute food intake was reduced by 15% in DU6 mice (P<0.001) but not in Fzt:DU mice. In both mouse lines feeding of the high fat diet elevated body mass if compared to the control diet (P<0.05). In contrast to controls, DU6 mice did not display high fat diet-induced increases of epididymal and renal fat. Control mice progressively developed glucose intolerance with advancing age and even more in response to the high fat diet. In contrast, obese DU6 mice did neither develop a glucose intolerant phenotype with progressive age nor when challenged with a high fat diet. Conclusions/Interpretation Our results from a polygenic mouse model demonstrate that genetically pre-determined and life-long obesity is no precondition of glucose intolerance later in life. PMID:24236159

Brenmoehl, Julia; Walz, Christina; Zeissler, Anja; Tuchscherer, Armin; Piechotta, Marion; Wiesner, Rudolf J.; Bielohuby, Maximilian; Hoeflich, Andreas

2013-01-01

57

Exposure to Common Food Additive Carrageenan Alone Leads to Fasting Hyperglycemia and in Combination with High Fat Diet Exacerbates Glucose Intolerance and Hyperlipidemia without Effect on Weight  

PubMed Central

Aims. Major aims were to determine whether exposure to the commonly used food additive carrageenan could induce fasting hyperglycemia and could increase the effects of a high fat diet on glucose intolerance and dyslipidemia. Methods. C57BL/6J mice were exposed to either carrageenan, high fat diet, or the combination of high fat diet and carrageenan, or untreated, for one year. Effects on fasting blood glucose, glucose tolerance, lipid parameters, weight, glycogen stores, and inflammation were compared. Results. Exposure to carrageenan led to glucose intolerance by six days and produced elevated fasting blood glucose by 23 weeks. Effects of carrageenan on glucose tolerance were more severe than from high fat alone. Carrageenan in combination with high fat produced earlier onset of fasting hyperglycemia and higher glucose levels in glucose tolerance tests and exacerbated dyslipidemia. In contrast to high fat, carrageenan did not lead to weight gain. In hyperinsulinemic, euglycemic clamp studies, the carrageenan-exposed mice had higher early glucose levels and lower glucose infusion rate and longer interval to achieve the steady-state. Conclusions. Carrageenan in the Western diet may contribute to the development of diabetes and the effects of high fat consumption. Carrageenan may be useful as a nonobese model of diabetes in the mouse.

Bhattacharyya, Sumit; Feferman, Leo; Unterman, Terry; Tobacman, Joanne K.

2015-01-01

58

Validation of capillary glucose measurements to detect glucose intolerance or type 2 diabetes mellitus in the general population  

Microsoft Academic Search

Background: The use of an oral glucose tolerance test (OGTT) has been recommended to diagnose type 2 diabetes, but an OGTT with venous blood sampling may not be feasible in the screening phase preceding large epidemiological studies. We have conducted a population-based screening in 2715 men and women and evaluated the diagnostic validity of capillary plasma glucose concentration measurements versus

Margriet Kruijshoop; Edith J. M. Feskens; Ellen E. Blaak; Tjerk W. A. de Bruin

2004-01-01

59

Differences in insulin and sympathetic responses to glucose ingestion due to family history of hypertension  

Microsoft Academic Search

To evaluate the relationship of metabolic and neural factors in familial hypertention, we examined blood pressure (BP), blood glucose, and plasma insulin and norepinephrine (NE) levels before and every 30 min for 120 min after glucose ingestion in six groups with 20 subjects each: normotensive subjects (NT) with and without a family history of hypertension; borderline hypertensive patients (BHT) with

Kazuko Masuo; Hiroshi Mikami; Toshio Ogihara; Michael L. Tuck

1996-01-01

60

Prediction of glucose intolerance at 24-28 weeks of gestation by glucose and insulin level measurements in the first trimester  

PubMed Central

Background: Gestational diabetes is the second common disorder in pregnancy period, which is detected in 24-28 weeks of gestational age through screening tests in low-risk women. The women with gestational diabetes are prone to prenatal mortality and development of future diabetes. Therefore, detection of these individuals in the first trimester and conducting preventive interventions is of great importance. This study aimed to define the predictive value of fasting plasma glucose (FPG) and fasting plasma insulin (FPI) test in first trimester concerning the positive result of oral glucose challenge test (OGCT). Materials and Methods: This is a prospective and observational study conducted on 88 pregnant women in Tehran. After FPG and FPI measurements in these women in the first trimester, a screening test of GCT with 50 g oral glucose was conducted in 24-28 weeks of gestational age. Diagnostic value of FPG and in these two groups of positive and normal GCT results was evaluated through receiver operator characteristic (ROC) curve. P < 0.05 was considered significant. Results: In this study, 15 subjects (17%) were detected with a positive GCT result. The sub-curve area of ROC diagram for FPG and FPI was calculated to be 0.573and 0.592, respectively, which reveals that FPG and FPI cannot have a proper predictive value for the positive result of GCT. Based on the results, the best cutoff points for FPG and FPI are 79.5 mg/dl and 7.55 ?IU/ml, with accuracy of 60-67% and specificity of 45.2-47%. Conclusions: Only higher fasting glucose levels in early pregnancy, within the normoglycemic range, would predict the development of glucose intolerance with limited sensitivity and specificity. PMID:25709695

Fahami, Fariba; Torabi, Sahar; Abdoli, Samereh

2015-01-01

61

Hepatic Branch Vagus Nerve Plays a Critical Role in the Recovery of Post-Ischemic Glucose Intolerance and Mediates a Neuroprotective Effect by Hypothalamic Orexin-A  

PubMed Central

Orexin-A (a neuropeptide in the hypothalamus) plays an important role in many physiological functions, including the regulation of glucose metabolism. We have previously found that the development of post-ischemic glucose intolerance is one of the triggers of ischemic neuronal damage, which is suppressed by hypothalamic orexin-A. Other reports have shown that the communication system between brain and peripheral tissues through the autonomic nervous system (sympathetic, parasympathetic and vagus nerve) is important for maintaining glucose and energy metabolism. The aim of this study was to determine the involvement of the hepatic vagus nerve on hypothalamic orexin-A-mediated suppression of post-ischemic glucose intolerance development and ischemic neuronal damage. Male ddY mice were subjected to middle cerebral artery occlusion (MCAO) for 2 h. Intrahypothalamic orexin-A (5 pmol/mouse) administration significantly suppressed the development of post-ischemic glucose intolerance and neuronal damage on day 1 and 3, respectively after MCAO. MCAO-induced decrease of hepatic insulin receptors and increase of hepatic gluconeogenic enzymes on day 1 after was reversed to control levels by orexin-A. This effect was reversed by intramedullary administration of the orexin-1 receptor antagonist, SB334867, or hepatic vagotomy. In the medulla oblongata, orexin-A induced the co-localization of cholin acetyltransferase (cholinergic neuronal marker used for the vagus nerve) with orexin-1 receptor and c-Fos (activated neural cells marker). These results suggest that the hepatic branch vagus nerve projecting from the medulla oblongata plays an important role in the recovery of post-ischemic glucose intolerance and mediates a neuroprotective effect by hypothalamic orexin-A. PMID:24759941

Harada, Shinichi; Yamazaki, Yui; Koda, Shuichi; Tokuyama, Shogo

2014-01-01

62

Secretory granule neuroendocrine protein 1 (SGNE1) genetic variation and glucose intolerance in severe childhood and adult obesity  

PubMed Central

Background 7B2 is a regulator/activator of the prohormone convertase 2 which is involved in the processing of numerous neuropeptides, including insulin, glucagon and pro-opiomelanocortin. We have previously described a suggestive genetic linkage peak with childhood obesity on chr15q12-q14, where the 7B2 encoding gene, SGNE1 is located. The aim of this study is to analyze associations of SGNE1 genetic variation with obesity and metabolism related quantitative traits. Methods We screened SGNE1 for genetic variants in obese children and genotyped 12 frequent single nucleotide polymorphisms (SNPs). Case control analyses were performed in 1,229 obese (534 children and 695 adults), 1,535 individuals with type 2 diabetes and 1,363 controls, all French Caucasians. We also studied 4,922 participants from the D.E.S.I.R prospective population-based cohort. Results We did not find any association between SGNE1 SNPs and childhood or adult obesity. However, the 5' region SNP -1,701A>G associated with higher area under glucose curve after oral glucose tolerance test (p = 0.0005), higher HOMA-IR (p = 0.005) and lower insulinogenic index (p = 0.0003) in obese children. Similar trends were found in obese adults. SNP -1,701A>G did not associate with risk of T2D but tends to associate with incidence of type 2 diabetes (HR = 0.75 95%CI [0.55–1.01]; p = 0.06) in the prospective cohort. Conclusion SGNE1 genetic variation does not contribute to obesity and common forms of T2D but may worsen glucose intolerance and insulin resistance, especially in the background of severe and early onset obesity. Further molecular studies are required to understand the molecular bases involved in this process. PMID:17617923

Bouatia-Naji, Nabila; Vatin, Vincent; Lecoeur, Cécile; Heude, Barbara; Proença, Christine; Veslot, Jacques; Jouret, Béatrice; Tichet, Jean; Charpentier, Guillaume; Marre, Michel; Balkau, Beverley; Froguel, Philippe; Meyre, David

2007-01-01

63

Verapamil Reverses Glucose Intolerance in Preexisting Chronic Renal Failure: Studies on Mechanisms  

Microsoft Academic Search

Glucose-induced insulin secretion is impaired in chronic renal failure (CRF), and this abnormality is due to the elevation of cytosolic calcium [Ca2+]i and other derangements in pancreatic islet metabolism. Verapamil given to rats from day 1 of CRF prevented the rise in [Ca2+]i of islets and the impairment in insulin secretion. However, it is not known whether verapamil can reverse

Prasert Thanakitcharu; George Z. Fadda; Suha M. Hajjar; Edi Levi; Olivera Stojceva-Taneva; Shaul G. Massry

1992-01-01

64

Chromium Alleviates Glucose Intolerance, Insulin Resistance, and Hepatic ER Stress in Obese Mice  

Microsoft Academic Search

Objective:Chromium has gained popularity as a nutritional supplement for diabetic patients. This study evaluated the effect of chronic administration of a chromium complex of D-phenylalanine (Cr(D-phe)3) on glucose and insulin tolerance in obese mice. The study tested the hypothesis that Cr(D-phe)3 suppresses endoplasmic reticulum (ER) stress and insulin resistance in these animals.Methods and Procedures:C57BL lean and ob\\/ob obese mice were

Nair Sreejayan; Feng Dong; Machender R. Kandadi; Xiaoping Yang; Jun Ren

2008-01-01

65

Lactose intolerance  

MedlinePLUS

Lactase deficiency; Milk intolerance; Disaccharidase deficiency; Dairy product intolerance ... make the lactase enzyme so they can digest milk, including breast milk. Babies born too early (premature) ...

66

Differences in insulin and sympathetic responses to glucose ingestion due to family history of hypertension.  

PubMed

To evaluate the relationship of metabolic and neural factors in familial hypertension, we examined blood pressure (BP), blood glucose, and plasma insulin and norepinephrine (NE) levels before and every 30 min for 120 min after glucose ingestion in six groups with 20 subjects each: normotensive subjects (NT) with and without a family history of hypertension; borderline hypertensive patients (BHT) with and without a family history of hypertension; and established hypertensive patients (EH) with and without a family history of hypertension. The changes in blood glucose were similar in the six groups. In the subjects with a positive family history of hypertension regardless of BP levels, the basal levels and changes in insulin levels after glucose ingestion were significantly greater than those in the subjects without a family history of hypertension (F = 13.32, P = .0001). In BHT and EH subjects, regardless of family history, changes in insulin were greater than in NT (F = 16.00, P = .0001). Basal levels and changes in plasma NE were higher in BHT and EH (F = 26.55, P = .0001) than NT and changes in plasma NE were greater in subjects with a family history than those in subjects without a family history (F = 18.32, P = .0001). Thus, abnormal insulin and NE responses to glucose appear to aggregate in subjects with a history of familial hypertension, regardless of the level of BP. Furthermore, the ratio of delta NE/ delta insulin (changes from basal to peak) in NT and BHT, and in subjects with a family history were significantly greater than in EH and in subjects without a family history. Thus, we demonstrated that concomitant abnormalities in the glucose-insulin regulatory system and the sympathetic nervous system characterize the early phase in the development of hypertension and these abnormalities have an apparent genetic basis. PMID:8862219

Masuo, K; Mikami, H; Ogihara, T; Tuck, M L

1996-08-01

67

Potential probiotic Bifidobacterium animalis ssp. lactis 420 prevents weight gain and glucose intolerance in diet-induced obese mice.  

PubMed

Alterations of the gut microbiota and mucosal barrier are linked with metabolic diseases. Our aim was to investigate the potential benefit of the potential probiotic Bifidobacterium animalis ssp. lactis 420 in reducing high-fat diet-induced body weight gain and diabetes in mice. In the obesity model, C57Bl/6J mice were fed a high-fat diet (60 energy %) for 12 weeks, and gavaged daily with B. lactis 420 (109 cfu) or vehicle. In the diabetes model, mice were fed a high-fat, ketogenic diet (72 energy % fat) for 4 weeks, with a 6-week subsequent treatment with B. lactis 420 (108-1010 cfu/day) or vehicle, after which they were analysed for body composition. We also analysed glucose tolerance, plasma lipopolysaccharide and target tissue inflammation using only one of the B. lactis 420 groups (109 cfu/day). Intestinal bacterial translocation and adhesion were analysed in a separate experiment using an Escherichia coli gavage. Body fat mass was increased in both obese (10.7 ± 0.8 g (mean ± standard error of mean) vs. 1.86 ± 0.21 g, P<0.001) and diabetic mice (3.01 ± 0.4 g vs. 1.14 ± 0.15 g, P<0.001) compared to healthy controls. Treatment with B. lactis 420 significantly decreased fat mass in obese (7.83 ± 0.67 g, P=0.007 compared to obese with vehicle) and diabetic mice (1.89 ± 0.16 g, P=0.02 for highest dose). This was reflected as reduced weight gain and improved glucose tolerance. Furthermore, B. lactis 420 decreased plasma lipopolysaccharide levels (P<0.001), liver inflammation (P=0.04), and E. coli adhesion in the distal gut (P<0.05). In conclusion, B. lactis 420 reduces fat mass and glucose intolerance in both obese and diabetic mice. Reduced intestinal mucosal adherence and plasma lipopolysaccharide suggest a mechanism related to reduced translocation of gut microbes. PMID:25062610

Stenman, L K; Waget, A; Garret, C; Klopp, P; Burcelin, R; Lahtinen, S

2014-12-01

68

Inhibition of adipogenesis and development of glucose intolerance by soluble preadipocyte factor–1 (Pref-1)  

PubMed Central

Preadipocyte factor-1 (Pref-1) is a transmembrane protein highly expressed in preadipocytes. Pref-1 expression is, however, completely abolished in adipocytes. The extracellular domain of Pref-1 undergoes two proteolytic cleavage events that generate 50 and 25 kDa soluble products. To understand the function of Pref-1, we generated transgenic mice that express the full ectodomain corresponding to the large cleavage product of Pref-1 fused to human immunoglobulin-? constant region. Mice expressing the Pref-1/hFc transgene in adipose tissue, driven by the adipocyte fatty acid–binding protein (aP2, also known as aFABP) promoter, showed a substantial decrease in total fat pad weight. Moreover, adipose tissue from transgenic mice showed reduced expression of adipocyte markers and adipocyte-secreted factors, including leptin and adiponectin, whereas the preadipocyte marker Pref-1 was increased. Pref-1 transgenic mice with a substantial, but not complete, loss of adipose tissue exhibited hypertriglyceridemia, impaired glucose tolerance, and decreased insulin sensitivity. Mice expressing the Pref-1/hFc transgene exclusively in liver under the control of the albumin promoter also showed a decrease in adipose mass and adipocyte marker expression, suggesting an endocrine mode of action of Pref-1. These findings demonstrate the inhibition of adipogenesis by Pref-1 in vivo and the resulting impairment of adipocyte function that leads to the development of metabolic abnormalities. PMID:12588883

Lee, Kichoon; Villena, Josep A.; Moon, Yang Soo; Kim, Kee-Hong; Lee, Sunjoo; Kang, Chulho; Sul, Hei Sook

2003-01-01

69

Increased Myocardial Uptake of Dietary Fatty Acids Linked to Cardiac Dysfunction in Glucose-Intolerant Humans  

PubMed Central

Impaired cardiac systolic and diastolic function has been observed in preclinical models and in subjects with type 2 diabetes. Using a recently validated positron emission tomography (PET) imaging method with 14(R,S)-[18F]-fluoro-6-thia-heptadecanoic acid to quantify organ-specific dietary fatty acid partitioning, we demonstrate in this study that overweight and obese subjects with impaired glucose tolerance (IGT+) display significant increase in fractional myocardial dietary fatty acid uptake over the first 6 h postprandial compared with control individuals (IGT?). Measured by [11C]acetate with PET, IGT+ subjects have a significant increase in myocardial oxidative index. IGT+ subjects have significantly reduced left ventricular stroke volume and ejection fraction (LVEF) and tend to display impaired diastolic function, as assessed by PET ventriculography. We demonstrate an inverse relationship between increased myocardial dietary fatty acid partitioning and LVEF. Fractional dietary fatty acid uptake is reduced in subcutaneous abdominal and visceral adipose tissues in IGT+ directly associated with central obesity. Fractional dietary fatty acid uptake in skeletal muscles or liver is, however, similar in IGT+ versus IGT?. The current study demonstrates, for the first time, that excessive myocardial partitioning of dietary fatty acids occurs in prediabetic individuals and is associated with early impairment of left ventricular function and increased myocardial oxidative metabolism. PMID:23093657

Labbé, Sébastien M.; Grenier-Larouche, Thomas; Noll, Christophe; Phoenix, Serge; Guérin, Brigitte; Turcotte, Eric E.; Carpentier, André C.

2012-01-01

70

Biphasic effect of epinephrine on blood glucose during hyperinsulinemiain borderline hypertensive young men  

Microsoft Academic Search

We aimed to study the glycemic response to epinephrine during hyperinsulinemia and infused epinephrine (0.03 ?g\\/kg\\/min) for 30 min after 90 min of hyperinsulinemic glucose clamp in 14 borderline hypertensive young men. Plasma epinephrine was increased from 0.34 ± 0.08 to 2.33 ± 0.33 nmol\\/L while insulin and glucose infusions were kept constant with consequent changes in blood glucose. Initially

Aud Høieggen; Eigil Fossum; Andreas Moan; Morten Rostrup; Ivar K. Eide; Sverre E. Kjeldsen

2001-01-01

71

Reversal of glucose intolerance in rat offspring exposed to ethanol before birth through reduction of nuclear skeletal muscle HDAC expression by the bile acid TUDCA  

PubMed Central

Abstract Prenatal ethanol exposure causes cellular stress, insulin resistance, and glucose intolerance in adult offspring, with increased gluconeogenesis and reduced muscle glucose transporter?4 (glut4) expression. Impaired insulin activation of Akt and nuclear translocation of histone deacetylases (HDACs) in the liver partly explain increased gluconeogenesis. The mechanism for the reduced glut4 is unknown. Pregnant rats were gavaged with ethanol over the last week of gestation and adult female offspring were studied. Some ethanol exposed offspring was treated with tauroursodeoxycholic acid (TUDCA) for 3 weeks. All these rats underwent intraperitoneal glucose tolerance and insulin tolerance tests. The expression of glut4, HDACs, and markers of endoplasmic reticulum (ER) unfolded protein response (XBP1, CHOP, ATF6) was examined in the gastrocnemius muscle fractions, and in C2C12 muscle cells cultured with ethanol, TUDCA, and HDAC inhibitors. Non?TUDCA?treated rats exposed to prenatal ethanol were insulin resistant and glucose intolerant with reduced muscle glut4 expression, increased ER marker expression, and increased nuclear HDACs, whereas TUDCA?treated rats had normal insulin sensitivity and glucose tolerance with normal glut4 expression, ER marker expression, and HDAC levels. In C2C12 cells, ethanol reduced glut4 expression, but increased ER makers. While TUDCA restored glut4 and ER markers to control levels and HDAC inhibition rescued glut4 expression, HDAC inhibition had no effect on ER markers. The increase in nuclear HDAC levels consequent to prenatal ethanol exposure reduces glut4 expression in adult rat offspring, and this HDAC effect is independent of ER unfolded protein response. HDAC inhibition by TUDCA restores glut4 expression, with improvement in insulin sensitivity and glucose tolerance. PMID:25538147

Yao, Xing?Hai; Nguyen, Khanh H.; Nyomba, B. L. Grégoire

2014-01-01

72

Carbenoxolone Treatment Ameliorated Metabolic Syndrome in WNIN/Ob Obese Rats, but Induced Severe Fat Loss and Glucose Intolerance in Lean Rats  

PubMed Central

Background 11beta-hydroxysteroid dehydrogenase type 1 (11?-HSD1) regulates local glucocorticoid action in tissues by catalysing conversion of inactive glucocorticoids to active glucocorticoids. 11?-HSD1 inhibition ameliorates obesity and associated co-morbidities. Here, we tested the effect of 11?-HSD inhibitor, carbenoxolone (CBX) on obesity and associated comorbidities in obese rats of WNIN/Ob strain, a new animal model for genetic obesity. Methodology/Principal Findings Subcutaneous injection of CBX (50 mg/kg body weight) or volume-matched vehicle was given once daily for four weeks to three month-old WNIN/Ob lean and obese rats (n?=?6 for each phenotype and for each treatment). Body composition, plasma lipids and hormones were assayed. Hepatic steatosis, adipose tissue morphology, inflammation and fibrosis were also studied. Insulin resistance and glucose intolerance were determined along with tissue glycogen content. Gene expressions were determined in liver and adipose tissue. CBX significantly inhibited 11?-HSD1 activity in liver and adipose tissue of WNIN/Ob lean and obese rats. CBX significantly decreased body fat percentage, hypertriglyceridemia, hypercholesterolemia, insulin resistance in obese rats. CBX ameliorated hepatic steatosis, adipocyte hypertrophy, adipose tissue inflammation and fibrosis in obese rats. Tissue glycogen content was significantly decreased by CBX in liver and adipose tissue of obese rats. Severe fat loss and glucose- intolerance were observed in lean rats after CBX treatment. Conclusions/Significance We conclude that 11?-HSD1 inhibition by CBX decreases obesity and associated co-morbidities in WNIN/Ob obese rats. Our study supports the hypothesis that inhibition of 11?-HSD1 is a key strategy to treat metabolic syndrome. Severe fat loss and glucose -intolerance by CBX treatment in lean rats suggest that chronic 11?-HSD1 inhibition may lead to insulin resistance in normal conditions. PMID:23284633

Prasad Sakamuri, Siva Sankara Vara; Sukapaka, Mahesh; Prathipati, Vijay Kumar; Nemani, Harishankar; Putcha, Uday Kumar; Pothana, Shailaja; Koppala, Swarupa Rani; Ponday, Lakshmi Raj Kumar; Acharya, Vani; Veetill, Giridharan Nappan; Ayyalasomayajula, Vajreswari

2012-01-01

73

Lactose Intolerance  

MedlinePLUS

... Buy IFFGD Merchandise Take Action Contact Us Donate Lactose Intolerance Lactose is a sugar found in milk and other dairy products. Lactose intolerance is a condition where symptoms occur after digesting ...

74

Lactose Intolerance  

MedlinePLUS

... absorbed into the bloodstream and turned into energy — fuel for our bodies. People with lactose intolerance do ... who are lactose intolerant come up with eating alternatives and develop a well-balanced diet that provides ...

75

Glucose intolerance in aging male IGFBP-3 transgenic mice: differential effects of human IGFBP-3 and its mutant IGFBP-3 devoid of IGF binding ability.  

PubMed

We have reported a reduction of insulin secretion and glucose intolerance in young mice overexpressing human IGFBP-3 (phosphoglycerate kinase [PGK]BP3) or its mutant Gly56/Gly80/Gly81-IGFBP-3 (PGKmutBP3) under the PGK promoter. Here, we investigated changes in glucose and lipid homeostasis with age in PGKBP3 and PGKmutBP3 mice compared with wild-type mice. Body weight, glucose tolerance, insulin tolerance, visceral fat, interscapular brown adipose tissue (BAT), serum lipids, and pancreas histology were examined at age 3, 6, and 12 months. Murine IGFBP-3 was similar in all mouse genotypes and decreased with age in parallel with total IGF-1. Visceral fat and BAT masses increased in PGKmutBP3 mice, but not in PGKBP3 mice. Glucose tolerance was impaired in both PGKBP3 and PGKmutBP3 mice. However, PGKBP3 mice had increased expression of uncoupling protein-1 in BAT and reduced adiposity, and continued to have smaller pancreatic ?-cell mass and reduced insulin secretion through age 12 months. In contrast, PGKmutBP3 mice developed insulin resistance with age in association with pancreatic ?-cell hyperplasia, impaired expression of uncoupling protein-1 in BAT, and increased adiposity. In addition, both PGKBP3 and PGKmutBP3 mice had elevated glycerol in the circulation, but only PGKBP3 mice had elevated free fatty acids and only PGKmutBP3 mice had elevated triglycerides. Estimated free IGF-1 did not increase with age in transgenic mice, as it did in wild-type mice. Thus, overexpression of human IGFBP-3 or its mutant devoid of IGF binding ability leads to glucose intolerance with, however, different effects on insulin secretion, insulin sensitivity, and lipid homeostasis in aging mice. PMID:25490144

Nguyen, K Hoa; Yao, Xing-Hai; Erickson, Adam G; Mishra, Suresh; Nyomba, B L Grégoire

2015-02-01

76

The Glucose Tolerance Test, But Not HbA 1c, Remains the Gold Standard in Identifying Unrecognized Diabetes Mellitus and Impaired Glucose Tolerance in Hypertensive Subjects  

Microsoft Academic Search

The objective of this study was to compare the value of the oral glucose tolerance test (GTT), glycated hemoglobin concentration (HbA1c), and fasting plasma glucose (FPG) for identifying unrecognized diabetes mellitus (DM) and impaired glucose tolerance (IGT) in hypertensive subjects. One hundred forty-four consecutive subjects who were not known to have DM and who were attending the Hypertension Clinic underwent

Abdul-Majeed Salmasi; Mark Dancy

2005-01-01

77

The relationship between abnormal glucose tolerance and hypertensive disorders of pregnancy in healthy nulliparous women  

Microsoft Academic Search

Objective: The study’s aim was to determine whether healthy nulliparous women with abnormal glucose tolerance during pregnancy are at increased risk for development of pregnancy-associated hypertension or preeclampsia. Study Design: A series of 4589 healthy nulliparous women from 5 university centers were evaluated prospectively to determine whether calcium supplementation would prevent preeclampsia. Pregnancy-associated hypertension was a diastolic blood pressure ?90

Gary M. Joffe; Joy R. Esterlitz; Richard J. Levine; John D. Clemens; Marian G. Ewell; Baha M. Sibai; Patrick M. Catalano

1998-01-01

78

The association between daily physical activity and plasma B-type natriuretic peptide in patients with glucose intolerance: a cross-sectional study  

PubMed Central

Objectives In spite of accumulating evidences suggesting an inverse association between insulin resistance and plasma B-type natriuretic peptide (BNP) levels, the effect of daily physical activity on plasma BNP in individuals with glucose intolerance remains unknown. We investigated the association of physical activity level (PAL) with plasma BNP in patients with impaired fasting glucose, impaired glucose tolerance and type 2 diabetes. Design Cross-sectional study. Setting Outpatients visiting the National Center for Global Health and Medicine Kohnodai Hospital. Participants A total of 60 patients with glucose intolerance who did not take any hypoglycaemic agents, cholesterol-lowering agents and antihypertensive agents were recruited. Patients who were diagnosed as having heart failure and renal impairment, engaged in sports-like exercise and resistance training were excluded. Primary outcome measures PAL was objectively measured by a triaxial accelerometer. The association between PAL and plasma BNP levels was assessed by multiple regression analysis. Results PAL was positively correlated with plasma BNP levels (r=0.296, p=0.021). PAL was still significantly correlated with plasma BNP levels after adjustment for age (?=0.290, p=0.014), and adjustment for age and body mass index (?=0.282, p=0.018). Plasma BNP levels were inversely correlated with serum insulin levels (r=?0.350, p=0.006) and homeostasis model assessment-estimated insulin resistance (HOMA-IR; r=?0.363, p=0.004). Serum insulin levels (mean±SD, 8.1±6.4??U/mL) and HOMA-IR (2.4±1.9) in the high-BNP group were significantly lower than those (11.2±7.4??U/mL and 3.7±3.0, respectively) in the low-BNP group. Conclusions Our findings propose the possibility that plasma BNP may be increased by daily physical activity and BNP is associated with insulin resistance. PMID:25596197

Hamasaki, Hidetaka; Yanai, Hidekatsu; Kakei, Masafumi; Noda, Mitsuhiko; Ezaki, Osamu

2015-01-01

79

Hypertension and insulin disorders  

Microsoft Academic Search

Insulin resistance and\\/or compensatory hyperinsulinemia are associated with hypertension, obesity, dyslipidemia, and glucose\\u000a intolerance. Insulin resistance and hyperinsulinemia are considered to increase blood pressure through sympathetic nervous\\u000a system activation, renin-angiotensin system stimulation, and vascular smooth muscle cell proliferation. Leptin, magnesium\\u000a ions, nitric oxide, endothelin, peroxisome proliferator-activated receptor ?, and tumor necrosis factor-? also modulate blood\\u000a pressure. Decreasing insulin resistance by

Michinori Imazu

2002-01-01

80

Voluntary running improves glucose tolerance and insulin resistance in female spontaneously hypertensive rats  

Microsoft Academic Search

We evaluated the effects of voluntary exercise training on glucose metabolism and measures of insulin sensitivity in female spontaneously hypertensive rats (SHR). Age-matched Wistar-Kyoto rats (WKY) were used as normotensive controls. Exercising SHR were housed in running wheels for 8 weeks (SHRx8) or 16 weeks (SHRx16). At 22 weeks of age, we measured systolic blood pressure, performed oral glucose tolerance

Tanya L. Kinney LaPier; Arthur L. M. Swislocki; Raymond J. Clark; Kenneth J. Rodnick

2001-01-01

81

Muscle-specific Pikfyve gene disruption causes glucose intolerance, insulin resistance, adiposity, and hyperinsulinemia but not muscle fiber-type switching  

PubMed Central

The evolutionarily conserved kinase PIKfyve that synthesizes PtdIns5P and PtdIns(3,5)P2 has been implicated in insulin-regulated GLUT4 translocation/glucose entry in 3T3-L1 adipocytes. To decipher PIKfyve's role in muscle and systemic glucose metabolism, here we have developed a novel mouse model with Pikfyve gene disruption in striated muscle (MPIfKO). These mice exhibited systemic glucose intolerance and insulin resistance at an early age but had unaltered muscle mass or proportion of slow/fast-twitch muscle fibers. Insulin stimulation of in vivo or ex vivo glucose uptake and GLUT4 surface translocation was severely blunted in skeletal muscle. These changes were associated with premature attenuation of Akt phosphorylation in response to in vivo insulin, as tested in young mice. Starting at 10–11 wk of age, MPIfKO mice progressively accumulated greater body weight and fat mass. Despite increased adiposity, serum free fatty acid and triglyceride levels were normal until adulthood. Together with the undetectable lipid accumulation in liver, these data suggest that lipotoxicity and muscle fiber switching do not contribute to muscle insulin resistance in MPIfKO mice. Furthermore, the 80% increase in total fat mass resulted from increased fat cell size rather than altered fat cell number. The observed profound hyperinsulinemia combined with the documented increases in constitutive Akt activation, in vivo glucose uptake, and gene expression of key enzymes for fatty acid biosynthesis in MPIfKO fat tissue suggest that the latter is being sensitized for de novo lipid anabolism. Our data provide the first in vivo evidence that PIKfyve is essential for systemic glucose homeostasis and insulin-regulated glucose uptake/GLUT4 translocation in skeletal muscle. PMID:23673157

Ikonomov, Ognian C.; Sbrissa, Diego; Delvecchio, Khortnal; Feng, Han-Zhong; Cartee, Gregory D.; Jin, Jian-Ping

2013-01-01

82

Systemic Hypertension and Impaired Glucose Tolerance Are Independently Correlated to the Severity of the Acromegalic Cardiomyopathy  

Microsoft Academic Search

Increased mortality from cardiovascular diseases has been re- ported in acromegaly. Our objective was to evaluate the impact of glucose tolerance abnormalities and\\/or systemic hypertension in fur- ther worsening the acromegalic cardiomyopathy. The study design was open transversal. The subjects studied were 130 consecutive naive acromegalic patients (74 women and 56 men; age, 17- 80 yr). Interventricular septum (IST) and

ANNAMARIA COLAO; ROBERTO BALDELLI; PAOLO MARZULLO; ELISABETTA FERRETTI; DIEGO FERONE; PATRIZIA GARGIULO; MARIO PETRETTA; GUIDO TAMBURRANO; GAETANO LOMBARDI; ANTONIO LIUZZI

83

Long-term exposure to a high-fat diet results in the development of glucose intolerance and insulin resistance in interleukin-1 receptor I-deficient mice  

PubMed Central

Emerging evidence has demonstrated that saturated fatty acids prime pro-IL-1? production and inflammasome-mediated IL-1? activation is critical in obesity-associated insulin resistance (IR). Nonetheless, IL-1 receptor I-deficient (IL-1RI?/?) mice develop mature-onset obesity despite consuming a low-fat diet (LFD). With this apparent contradiction, the present study evaluated whether IL-1RI?/? mice were protected against long-term (6 mo) high-fat diet (HFD)-induced IR. Male wild-type and IL-1RI?/? mice were fed LFD or HFD for 3 or 6 mo, and glucose and insulin tolerance tests were performed. Adipose insulin sensitivity, cytokine profiles, and adipocyte morphology were assessed. The adipogenic potential of stromal vascular fraction was determined. Hepatic lipid accumulation and insulin sensitivity were characterized. IL-1RI?/? mice developed glucose intolerance and IR after 6 mo HFD compared with 3 mo HFD, coincident with enhanced weight gain, hyperinsulinemia, and hyperleptinemia. The aggravated IR phenotype was associated with loss of adipose functionality, switch from adipocyte hyperplasia to hypertrophy and hepatosteatosis. Induction of adipogenic genes was reduced in IL-1RI?/? preadipocytes after 6 mo HFD compared with 3 mo HFD. Obese LFD-IL-1RI?/? mice exhibited preserved metabolic health. IL-1RI?/? mice develop glucose intolerance and IR after 6 mo HFD intervention. While mature-onset obesity is evident in LFD-IL-1RI?/? mice, the additional metabolic insult of HFD was required to drive adipose inflammation and systemic IR. These findings indicate an important interaction between dietary fat and IL-1, relevant to optimal metabolic health. PMID:23921145

McGillicuddy, Fiona C.; Reynolds, Clare M.; Finucane, Orla; Coleman, Eilish; Harford, Karen A.; Grant, Christine; Sergi, Domenico; Williams, Lynda M.; Mills, Kingston H. G.

2013-01-01

84

Lactose Intolerance  

MedlinePLUS

... links Share this: Page Content What is lactose intolerance? People who are lactose intolerant have trouble digesting lactose, the natural sugar found in milk and milk products. They have this condition because their bodies do not make enough lactase. Lactase is an enzyme made in the small ...

85

Lactose Intolerance  

MedlinePLUS

... to absorb and turn into energy. People with lactose intolerance do not make enough lactase in their small intestine. Without lactase, the body ... while you're young. People can also develop lactose intolerance for other ... lactase. For example, people with inflammatory bowel disease (IBD) , ...

86

Prenatal Ethanol Exposure Causes Glucose Intolerance with Increased Hepatic Gluconeogenesis and Histone Deacetylases in Adult Rat Offspring: Reversal by Tauroursodeoxycholic Acid  

PubMed Central

Prenatal ethanol exposure results in increased glucose production in adult rat offspring and this may involve modulation of protein acetylation by cellular stress. We used adult male offspring of dams given ethanol during gestation days 1–7 (early), 8–14 (mid) and 15–21 (late) compared with those from control dams. A group of ethanol offspring was treated with tauroursodeoxycholic acid (TUDCA) for 3 weeks. We determined gluconeogenesis, phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphatase, hepatic free radicals, histone deacetylases (HDAC), acetylated foxo1, acetylated PEPCK, and C/EBP homologous protein as a marker of endoplasmic reticulum stress. Prenatal ethanol during either of the 3 weeks of pregnancy increased gluconeogenesis, gluconeogenic genes, oxidative and endoplasmic reticulum stresses, sirtuin-2 and HDAC3, 4, 5, and 7 in adult offspring. Conversely, prenatal ethanol reduced acetylation of foxo1 and PEPCK. Treatment of adult ethanol offspring with TUDCA reversed all these abnormalities. Thus, prenatal exposure of rats to ethanol results in long lasting oxidative and endoplasmic reticulum stresses explaining increased expression of gluconeogenic genes and HDAC proteins which, by deacetylating foxo1 and PEPCK, contribute to increased gluconeogenesis. These anomalies occurred regardless of the time of ethanol exposure during pregnancy, including early embryogenesis. As these anomalies were reversed by treatment of the adult offspring with TUDCA, this compound has therapeutic potentials in the treatment of glucose intolerance associated with prenatal ethanol exposure. PMID:23544086

Yao, Xing-Hai; Nguyen, Hoa K.; Nyomba, B. L. Grégoire

2013-01-01

87

Gs? deficiency in skeletal muscle leads to reduced muscle mass, fiber-type switching, and glucose intolerance without insulin resistance or deficiency  

PubMed Central

The ubiquitously expressed G protein ?-subunit Gs? is required for receptor-stimulated intracellular cAMP responses and is an important regulator of energy and glucose metabolism. We have generated skeletal muscle-specific Gs?-knockout (KO) mice (MGsKO) by mating Gs?-floxed mice with muscle creatine kinase-cre transgenic mice. MGsKO mice had normal body weight and composition, and their serum glucose, insulin, free fatty acid, and triglyceride levels were similar to that of controls. However, MGsKO mice were glucose intolerant despite the fact that insulin sensitivity and glucose-stimulated insulin secretion were normal, suggesting an insulin-independent mechanism. Isolated muscles from MGsKO mice had increased basal glucose uptake and normal responses to a stimulator of AMP-activated protein kinase (AMPK), which indicates that AMPK and its downstream pathways are intact. Compared with control mice, MGsKO mice had reduced muscle mass with decreased cross-sectional area and force production. In addition, adult MGsKO mice showed an increased proportion of type I (slow-twitch, oxidative) fibers based on kinetic properties and myosin heavy chain isoforms, despite the fact that these muscles had reduced expression of peroxisome proliferator-activated receptor coactivator protein-1? (PGC-1?) and reduced mitochondrial content and oxidative capacity. Therefore Gs? deficiency led to fast-to-slow fiber-type switching, which appeared to be dissociated from the expected change in oxidative capacity. MGsKO mice are a valuable model for future studies of the role of Gs? signaling pathways in skeletal muscle adaptation and their effects on whole body metabolism. PMID:19158402

Chen, Min; Feng, Han-Zhong; Gupta, Divakar; Kelleher, James; Dickerson, Kathryn E.; Wang, Jie; Hunt, Desmond; Jou, William; Gavrilova, Oksana; Jin, Jian-Ping; Weinstein, Lee S.

2009-01-01

88

Fish oil and argan oil intake differently modulate insulin resistance and glucose intolerance in a rat model of dietary-induced obesity.  

PubMed

We investigated the potential metabolic benefits of fish oil (FO) or vegetable argan oil (AO) intake in a dietary model of obesity-linked insulin resistance. Rats were fed a standard chow diet (controls), a high-fat/high-sucrose (HFHS) diet, or an HFHS diet in which 6% of the fat was replaced by either FO or AO feeding, respectively. The HFHS diet increased adipose tissue weight and insulin resistance as revealed by increased fasting glucose and exaggerated glycemic and insulin responses to a glucose tolerance test (intraperitoneal glucose tolerance test). Fish oil feeding prevented fat accretion, reduced fasting glycemia, and normalized glycemic or insulin responses to intraperitoneal glucose tolerance test as compared with HFHS diet. Unlike FO consumption, AO intake failed to prevent obesity, yet restored fasting glycemia back to chow-fed control values. Insulin-induced phosphorylation of Akt and Erk in adipose tissues, skeletal muscles, and liver was greatly attenuated in HFHS rats as compared with chow-fed controls. High-fat/high-sucrose diet-induced insulin resistance was also confirmed in isolated hepatocytes. Fish oil intake prevented insulin resistance by improving or fully restoring insulin signaling responses in all tissues and isolated hepatocytes. Argan oil intake also improved insulin-dependent phosphorylations of Akt and Erk; and in adipose tissue, these responses were increased even beyond values observed in chow-fed controls. Taken together, these results strongly support the beneficial action of FO on diet-induced insulin resistance and glucose intolerance, an effect likely explained by the ability of FO to prevent HFHS-induced adiposity. Our data also show for the first time that AO can improve some of the metabolic and insulin signaling abnormalities associated with HFHS feeding. PMID:19394055

Samane, Samira; Christon, Raymond; Dombrowski, Luce; Turcotte, Stéphane; Charrouf, Zoubida; Lavigne, Charles; Levy, Emile; Bachelard, Hélène; Amarouch, Hamid; Marette, André; Haddad, Pierre Selim

2009-07-01

89

Reduced nuclear protein 1 expression improves insulin sensitivity and protects against diet-induced glucose intolerance through up-regulation of heat shock protein 70.  

PubMed

We recently reported that deletion of the stress-regulated nuclear protein 1 (Nupr1) protected against obesity-associated metabolic alterations due to increased beta cell mass, but complete Nupr1 ablation was not advantageous since it led to insulin resistance on a normal diet. The current study used Nupr1 haplodeficient mice to investigate whether a partial reduction in Nupr1 expression conferred beneficial effects on glucose homeostasis. Islet number, morphology and area, assessed by immunofluorescence and morphometric analyses, were not altered in Nupr1 haplodeficient mice under normal diet conditions and nor was beta cell BrdU incorporation. Glucose and insulin tolerance tests indicated that there were no significant changes in in vivo insulin secretion and glucose clearance in Nupr1 haplodeficient mice, and beta cell function in vitro was normal. However, reduced Nupr1 expression decreased visceral fat deposition and significantly increased insulin sensitivity in vivo. In contrast to wild type animals, high fat diet-fed Nupr1 haplodeficient mice were not hyperinsulinaemic or glucose intolerant, and their sustained insulin sensitivity was demonstrated by appropriate insulin-induced Akt phosphorylation, as determined by Western blotting. At the molecular level, measurements of gene expression levels and promoter activities identified Nupr1-dependent inhibition of heat shock factor-1-induced heat shock protein 70 (Hsp70) expression as a mechanism through which Nupr1 regulates insulin sensitivity. We have shown for the first time that Nupr1 plays a central role in inhibiting Hsp70 expression in tissues regulating glucose homeostasis, and reductions in Nupr1 expression could be used to protect against the metabolic defects associated with obesity-induced insulin resistance. PMID:25638293

Barbosa-Sampaio, H C; Drynda, R; Liu, B; Rodriguez De Ledesma, A M; Malicet, C; Iovanna, J L; Jones, P M; Muller, D S; Persaud, S J

2015-05-01

90

Diagnostic criteria for diabetes mellitus and other categories of glucose intolerance: 1997 criteria by the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus (ADA), 1998 WHO Consultation criteria, and 1985 WHO criteria  

Microsoft Academic Search

To compare 1997 ADA diagnostic criteria for diabetes mellitus and other categories of glucose intolerance\\/1998 WHO Consultation criteria versus 1985 WHO criteria, we analyzed data from a 75-g oral glucose tolerance test (OGTT) performed on 1051 high-risk subjects without medical history of diabetes at Diabetes Screening Clinic, Ramathibodi Hospital, Thailand. There were 372 males and 679 females, aged (mean±S.D.)=50.3±12.55 years,

Gobchai Puavilai; Suwannee Chanprasertyotin; Aporn Sriphrapradaeng

1999-01-01

91

Free-Living Physical Activity Energy Expenditure Is Strongly Related to Glucose Intolerance in Cameroonian Adults Independently of Obesity  

PubMed Central

OBJECTIVE—We examined the cross-sectional association between objectively measured free-living physical activity energy expenditure (PAEE) and glucose tolerance in adult Cameroonians without known diabetes. RESEARCH DESIGN AND METHODS—PAEE was measured in 34 volunteers using the doubly labeled water method and indirect calorimetry (resting). Fasting blood glucose and 2-h postload blood glucose were measured during a standard 75-g oral glucose tolerance test. RESULTS—There was a significant negative correlation between PAEE and 2-h glucose (r = ?0.43; P = 0.01) but not fasting glucose (r = 0.1; P = 0.57). The inverse association between PAEE and 2-h glucose remained after adjustment for age, sex, smoking, alcohol consumption, and BMI (? = ?0.017 [95% CI ?0.033 to ?0.002]) and was unchanged after further adjustment for waist circumference, body fat percentage, or aerobic fitness. CONCLUSIONS—PAEE is inversely associated with 2-h glucose independently of adiposity or fitness. Interventions aimed at increasing PAEE could play an important role in diabetes prevention in developing countries. PMID:19017776

Assah, Felix K.; Ekelund, Ulf; Brage, Soren; Mbanya, Jean Claude; Wareham, Nicholas J.

2009-01-01

92

Oral Supplementation with Non-Absorbable Antibiotics or Curcumin Attenuates Western Diet-Induced Atherosclerosis and Glucose Intolerance in LDLR?/? Mice – Role of Intestinal Permeability and Macrophage Activation  

PubMed Central

Association between circulating lipopolysaccharide (LPS) and metabolic diseases (such as Type 2 Diabetes and atherosclerosis) has shifted the focus from Western diet-induced changes in gut microbiota per se to release of gut bacteria-derived products into circulation as the possible mechanism for the chronic inflammatory state underlying the development of these diseases. Under physiological conditions, an intact intestinal barrier prevents this release of LPS underscoring the importance of examining and modulating the direct effects of Western diet on intestinal barrier function. In the present study we evaluated two strategies, namely selective gut decontamination and supplementation with oral curcumin, to modulate Western-diet (WD) induced changes in intestinal barrier function and subsequent development of glucose intolerance and atherosclerosis. LDLR?/? mice were fed WD for 16 weeks and either received non-absorbable antibiotics (Neomycin and polymyxin) in drinking water for selective gut decontamination or gavaged daily with curcumin. WD significantly increased intestinal permeability as assessed by in vivo translocation of FITC-dextran and plasma LPS levels. Selective gut decontamination and supplementation with curcumin significantly attenuated the WD-induced increase in plasma LPS levels (3.32 vs 1.90 or 1.51 EU/ml, respectively) and improved intestinal barrier function at multiple levels (restoring intestinal alkaline phosphatase activity and expression of tight junction proteins, ZO-1 and Claudin-1). Consequently, both these interventions significantly reduced WD-induced glucose intolerance and atherosclerosis in LDLR?/? mice. Activation of macrophages by low levels of LPS (50 ng/ml) and its exacerbation by fatty acids is likely the mechanism by which release of trace amounts of LPS into circulation due to disruption of intestinal barrier function induces the development of these diseases. These studies not only establish the important role of intestinal barrier function, but also identify oral supplementation with curcumin as a potential therapeutic strategy to improve intestinal barrier function and prevent the development of metabolic diseases. PMID:25251395

Ghosh, Siddhartha S.; Bie, Jinghua; Wang, Jing; Ghosh, Shobha

2014-01-01

93

Fish oil ameliorates trimethylamine N-oxide-exacerbated glucose intolerance in high-fat diet-fed mice.  

PubMed

Trimethylamine N-oxide (TMAO), a component commonly present in seafood, has been found to have a harmful impact on glucose tolerance in high-fat diet (HFD)-fed mice. However, seafood also contains fish oil (FO), which has been shown to have beneficial effects on metabolism. Here, we investigated the effect of FO on TMAO-induced impaired glucose tolerance in HFD-fed mice. Male C57BL/6 mice were randomly assigned to the high fat (HF), TMAO, and fish oil groups. The HF group was fed a diet containing 25% fat, the TMAO group was fed the HFD plus 0.2% TMAO, and the FO group was fed the HFD plus 0.2% TMAO and 2% fish oil for 12 weeks. After 10 weeks of feeding, oral glucose tolerance tests were performed. Dietary FO improved the fasting glucose level, the fasting insulin level, HOMA-IR value, QUICKI score and ameliorated TMAO-induced exacerbated impaired glucose tolerance in HFD-fed mice. These effects were associated with the expression of genes related to the insulin signalling pathway, glycogen synthesis, gluconeogenesis, and glucose transport in peripheral tissues. Dietary fish oil also decreased TMAO-aggravated adipose tissue inflammation. Our results suggested that dietary FO ameliorated TMAO-induced impaired glucose tolerance, insulin signal transduction in peripheral tissue, and adipose tissue inflammation in HFD-fed mice. PMID:25686243

Gao, Xiang; Xu, Jie; Jiang, Chengzi; Zhang, Yi; Xue, Yong; Li, Zhaojie; Wang, Jingfeng; Xue, Changhu; Wang, Yuming

2015-04-01

94

Blood and urine responses to ingesting fluids of various salt and glucose concentrations. [to combat orthostatic intolerance  

NASA Technical Reports Server (NTRS)

To compensate for the reduced blood and fluid volumes that develop during weightlessness, the Space Shuttle crewmembers consume salt tablets and water equivalent to 1 l of normal saline, about 2 hrs before landing. This paper compares the effects on blood, urine, and cardiovascular variables of the ingestion of 1 l of normal (0.9 percent) saline with the effects of distilled water, 1 percent glucose, 0.74 percent saline with 1 percent glucose, 0.9 percent saline with 1 percent glucose, and 1.07 percent saline. It was found that the expansion of plasma volume and the concentration of urine were greater 4 hrs after ingestion of 1.07 percent saline solution than after ingestion of normal saline and that the solutions containig glucose did not enhance any variables as compared with normal saline.

Frey, Mary A.; Riddle, Jeanne; Charles, John B.; Bungo, Michael W.

1991-01-01

95

Body mass index, waist circumference, waist-hip ratio, and glucose intolerance in Chinese and Europid adults in Newcastle, UK.   

E-print Network

. METHODS: Population based samples of Chinese and European adults were recruited. Each subject had a standard WHO oral glucose tolerance test. RESULTS: Complete data were available for 375 Chinese and 610 Europid subjects. The age adjusted prevalences...

Unwin, Nigel; Harland, J; White, M; Bhopal, Raj; Winocour, P; Stephenson, P; Watson, W; Turner, C; Alberti, K G

1997-01-01

96

High glycosylated hemoglobin levels increase the risk of progression to diabetes mellitus in subjects with glucose intolerance  

Microsoft Academic Search

The relationships between HbA1c level and oral glucose tolerance test (OGTT) at the initial visit and the incidence of diabetes after 5 years of follow-up were investigated in 819 subjects participating in a general health examination. The 100 g OGTT was performed. In order to use WHO criteria, the blood glucose levels of 100 g OGTT corresponding to those of

Hideyo Yoshinaga; Kinori Kosaka

1996-01-01

97

Overexpression of Kinase-Negative Protein Kinase C? in Pancreatic ?-Cells Protects Mice From Diet-Induced Glucose Intolerance and ?-Cell Dysfunction  

PubMed Central

OBJECTIVE In vitro models suggest that free fatty acid–induced apoptotic ?-cell death is mediated through protein kinase C (PKC)?. To examine the role of PKC? signaling in vivo, transgenic mice overexpressing a kinase-negative PKC? (PKC?KN) selectively in ?-cells were generated and analyzed for glucose homeostasis and ?-cell survival. RESEARCH DESIGN AND METHODS Mice were fed a standard or high-fat diet (HFD). Blood glucose and insulin levels were determined after glucose loads. Islet size, cleaved caspase-3, and PKC? expression were estimated by immunohistochemistry. In isolated islet cells apoptosis was assessed with TUNEL/TO-PRO3 DNA staining and the mitochondrial potential by rhodamine-123 staining. Changes in phosphorylation and subcellular distribution of forkhead box class O1 (FOXO1) were analyzed by Western blotting and immunohistochemistry. RESULTS PKC?KN mice were protected from HFD-induced glucose intolerance. This was accompanied by increased insulin levels in vivo, by an increased islet size, and by a reduced staining of ?-cells for cleaved caspase-3 compared with wild-type littermates. In accordance, long-term treatment with palmitate increased apoptotic cell death of isolated islet cells from wild-type but not from PKC?KN mice. PKC?KN overexpression protected islet cells from palmitate-induced mitochondrial dysfunction and inhibited nuclear accumulation of FOXO1 in mouse islet and INS-1E cells. The inhibition of nuclear accumulation of FOXO1 by PKC?KN was accompanied by an increased phosphorylation of FOXO1 at Ser256 and a significant reduction of FOXO1 protein. CONCLUSIONS Overexpression of PKC?KN in ?-cells protects from HFD-induced ?-cell failure in vivo by a mechanism that involves inhibition of fatty acid–mediated apoptosis, inhibition of mitochondrial dysfunction, and inhibition of FOXO1 activation. PMID:19826167

Hennige, Anita M.; Ranta, Felicia; Heinzelmann, Isabel; Düfer, Martina; Michael, Diana; Braumüller, Heidi; Lutz, Stefan Z.; Lammers, Reiner; Drews, Gisela; Bosch, Fatima; Häring, Hans-Ulrich; Ullrich, Susanne

2010-01-01

98

Selective elevation of adiponectin production by the natural compounds derived from a medicinal herb alleviates insulin resistance and glucose intolerance in obese mice.  

PubMed

Adiponectin is an adipocyte-derived insulin-sensitizing hormone with antidiabetic, antiinflammatory, and antiatherosclerotic properties. A decreased serum level of adiponectin in obesity has been identified as an independent risk factor for diabetes and cardiovascular complications, suggesting that pharmacological intervention aimed at elevating adiponectin production might hold promise for the treatment and/or prevention of these diseases. Here we report the identification of two structurally related natural compounds (astragaloside II and isoastragaloside I) from the medicinal herb Radix Astragali that possess such an activity. Astragaloside II and isoastragaloside I selectively increased adiponectin secretion in primary adipocytes without any obvious effects on a panel of other adipokines. Furthermore, an additive effect on induction of adiponectin production was observed between these two compounds and rosiglitazone, a thiazolidinedione class of insulin-sensitizing drugs. Chronic administration of astragaloside II and isoastragaloside I in both dietary and genetic obese mice significantly elevated serum levels of total adiponectin and selectively increased the composition of its high molecular weight oligomeric complex. These changes were associated with an alleviation of hyperglycemia, glucose intolerance, and insulin resistance. By contrast, the beneficial effects of these two compounds on insulin sensitivity and glucose metabolism were diminished in adiponectin knockout mice. In conclusion, our results suggest that pharmacological elevation of circulating adiponectin alone is sufficient to ameliorate insulin resistance and diabetes and support the use of adiponectin as a biomarker for future drug discovery. The two natural compounds might provide the lead as a novel class of therapeutics for obesity-related diseases. PMID:18927219

Xu, Aimin; Wang, Hongbing; Hoo, Ruby L C; Sweeney, Gary; Vanhoutte, Paul M; Wang, Yu; Wu, Donghai; Chu, Wenjing; Qin, Guowei; Lam, Karen S L

2009-02-01

99

Segment of Rat Chromosome 20 Regulates Diet-Induced Augmentations in Adiposity, Glucose Intolerance, and Blood Pressure  

Microsoft Academic Search

Previous linkage and association studies have suggested that a region of human chromosome 6 containing the tumor necrosis factor (TNF)- gene is involved in the pathogenesis of obesity and obesity-associated hypertension. The aim of the present investigation was to establish whether a segment of rat chromosome 20 (RNO20), which also contains the TNF- gene, determines diet-induced changes in adiposity and

Zdenka Pausova; Lucie Sedova; Julie Berube; Pavel Hamet; Johanne Tremblay; Marc Dumont; Daniel Gaudet; Michal Pravenec; Vladimir Kren; Jaroslav Kunes

2010-01-01

100

Exercise training in the aerobic\\/anaerobic metabolic transition prevents glucose intolerance in alloxan-treated rats  

Microsoft Academic Search

BACKGROUND: Ninety percent of cases of diabetes are of the slowly evolving non-insulin-dependent type, or Type 2 diabetes. Lack of exercise is regarded as one of the main causes of this disorder. In this study we analyzed the effects of physical exercise on glucose homeostasis in adult rats with type 2 diabetes induced by a neonatal injection of alloxan. METHODS:

Clécia Soares de Alencar Mota; Carla Ribeiro; Gustavo Gomes de Araújo; Michel Barbosa de Araújo; Fúlvia de Barros Manchado-Gobatto; Fabrício Azevedo Voltarelli; Camila Aparecida Machado de Oliveira; Eliete Luciano; Maria de Mello

2008-01-01

101

Intrauterine protein restriction combined with early postnatal overfeeding was not associated with adult-onset obesity but produced glucose intolerance by pancreatic dysfunction  

PubMed Central

We investigated if whether intrauterine protein restriction in combination with overfeeding during lactation would cause adult-onset obesity and metabolic disorders. After birth, litters from dams fed with control (17% protein) and low protein (6% protein) diets were adjusted to a size of four (CO and LO groups, respectively) or eight (CC and LC groups, respectively) pups. All of the offspring were fed a diet containing 12% protein from the time of weaning until they were 90 d old. Compared to the CC and LC groups, the CO and LO groups had higher relative and absolute food intakes, oxygen consumption and carbon dioxide production; lower brown adipose tissue weight and lipid content and greater weight gain and absolute and relative white adipose tissue weight and absolute lipid content. Compared with the CO and CC rats, the LC and LO rats exhibited higher relative food intake, brown adipose tissue weight and lipid content, reduced oxygen consumption, carbon dioxide production and spontaneous activity, increased relative retroperitoneal adipose tissue weight and unaltered absolute white adipose tissue weight and lipid content. The fasting serum glucose was similar among the groups. The area under the glucose curve was higher in the LO and CO rats than in the LC and CC rats. The basal insulinemia and homeostasis model assessment of insulin resistance (HOMA-IR) were lower in the LO group than in the other groups. The total area under the insulin curve for the LO rats was similar to the CC rats, and both were lower than the CO and LC rats. Kitt was higher in the LO, LC and CO groups than in the CC group. Thus, intrauterine protein restriction followed by overfeeding during lactation did not induce obesity, but produced glucose intolerance by impairing pancreatic function in adulthood. PMID:23305533

2013-01-01

102

Lactose intolerance.  

PubMed

Persons with lactose intolerance are unable to digest significant amounts of lactose because of a genetically inadequate amount of the enzyme lactase. Common symptoms include abdominal pain and bloating, excessive flatus, and watery stool following the ingestion of foods containing lactose. Lactase deficiency is present in up to 15 percent of persons of northern European descent, up to 80 percent of blacks and Latinos, and up to 100 percent of American Indians and Asians. A sizable number of adults believe they are lactose intolerant but do not actually have impaired lactose digestion, and some persons with lactase deficiency can tolerate moderate amounts of ingested lactose. A diagnosis of lactose intolerance can usually be made with a careful history supported by dietary manipulation. If necessary, diagnosis can be confirmed by using a breath hydrogen or lactose tolerance test. Treatment consists primarily of avoiding lactose-containing foods. Lactase enzyme supplements may be helpful. The degree of lactose malabsorption varies greatly among patients with lactose intolerance, but most of them can ingest up to 12 oz of milk daily without symptoms. Lactose-intolerant patients must ensure adequate calcium intake. PMID:12018807

Swagerty, Daniel L; Walling, Anne D; Klein, Robert M

2002-05-01

103

The flavonoid-rich fraction of Coreopsis tinctoria promotes glucose tolerance regain through pancreatic function recovery in streptozotocin-induced glucose-intolerant rats  

Microsoft Academic Search

Aim of the studyInfusions of Coreopsis tinctoria Nutt. flowering tops have been used traditionally in Portugal to control hyperglycaemia and a previous study revealed that daily administration of the infusion during a 3-week period promoted the recovery of glucose tolerance by a mechanism different from inhibition of glucose absorption and direct promotion of insulin secretion.We know report the study of

Teresa Dias; Maria Rosário Bronze; Peter J. Houghton; Hélder Mota-Filipe; Alexandra Paulo

2010-01-01

104

Changes in plasma, erythrocyte, and platelet magnesium levels in normotensive and hypertensive obese subjects during oral glucose tolerance test  

Microsoft Academic Search

We evaluated the 75-g oral glucose tolerance test (OGTT)-induced modifications in glucose, insulin, and norepinephrine plasma concentrations, and in plasma, erythrocyte, and platelet magnesium levels in two groups of obese subjects (normotensive obese, NT-Ob, N = 19; hypertensive obese, HT-Ob, N = 15), and in a group of healthy control subjects (N = 12). During OGTT we detected a reduction

Francesco Corica; Alessandro Allegra; Riccardo Ientile; Michele Buemi; Andrea Corsonello; Salvatore Bonanzinga; Salvatore Macaione; Domenico Ceruso

1999-01-01

105

30 Year Patterns of Mortality in Tobago, West Indies, 1976-2005: Impact of Glucose Intolerance and Alcohol Intake  

PubMed Central

Objectives To determine the main predictors of all-cause and cardiovascular (CV) mortality in a rural West Indian population in Plymouth, Tobago over 30 years. Methods Questionnaire survey for CV risk factors and alcohol consumption patterns administered at baseline in 1976 with 92.5% response rate. 831/832 patients were followed up until 2005 or death. Results Hypertension (>140/90 mm Hg) was prevalent in 48% of men and 44% of women, and 21% of men and 17% of women had diabetes. Evidence showed most predictors for all cause and cardiovascular mortality having the main effects at ages <60 years, (p-value for interaction<0.01) but no risk factors having sex-specific effects on mortality. The main predictors of all-cause mortality at age <60 years in the fully adjusted model were high sessional alcohol intake (hazard ratio (HR) 2.04, 95% CI 1.10-3.80), severe hypertension >160/95 mm Hg (HR 1.68, 95% CI 1.09-2.60), diabetes (HR 3.28, 95% CI 1.89-5.69), and BMI (HR 1.04, 95% CI 1.00-1.07). The main predictors of cardiovascular mortality were similar in the fully adjusted model: high sessional alcohol intake (HR 2.47 95% CI 1.10-5.57), severe hypertension (HR 2.78 95% CI 1.56-4.95), diabetes (HR 3.68 95% CI 1.77-7.67) and additionally LVH, (HR 5.54 95% CI 1.38-22.26), however BMI did not show independent effects. For men, high sessional alcohol intake explains 27% of all cause mortality, and 40% of cardiovascular mortality at age <60 yrs. In adults aged <60 years, the attributable risk fraction for IGT/Diabetes and all cause mortality and cardiovascular mortality is 28% in women vs. 11% in men, and 22% in women vs. 6% in men respectively. Conclusions In this Afro-Caribbean population we found that a major proportion of deaths are attributable to high sessional alcohol intake (in males), diabetes, and hypertension and these risk factors primarily operate in those below 60 years. PMID:21283617

Molokhia, Mariam; Nitsch, Dorothea; Patrick, Alan Leslie; McKeigue, Paul

2011-01-01

106

Overexpression of PPAR? specifically in pancreatic ?-cells exacerbates obesity-induced glucose intolerance, reduces ?-cell mass, and alters islet lipid metabolism in male mice.  

PubMed

The contribution of peroxisomal proliferator-activated receptor (PPAR)-? agonism in pancreatic ?-cells to the antidiabetic actions of thiazolidinediones has not been clearly elucidated. Genetic models of pancreatic ?-cell PPAR? ablation have revealed a potential role for PPAR? in ?-cell expansion in obesity but a limited role in normal ?-cell physiology. Here we overexpressed PPAR?1 or PPAR?2 specifically in pancreatic ?-cells of mice subjected to high-fat feeding using an associated adenovirus (?-PPAR?1-HFD and ?-PPAR?2-HFD mice). We show ?-cell-specific PPAR?1 or PPAR?2 overexpression in diet-induced obese mice exacerbated obesity-induced glucose intolerance with decreased ?-cell mass, increased islet cell apoptosis, and decreased plasma insulin compared with obese control mice (?-eGFP-HFD mice). Analysis of islet lipid composition in ?-PPAR?2-HFD mice revealed no significant changes in islet triglyceride content and an increase in only one of eight ceramide species measured. Interestingly ?-PPAR?2-HFD islets had significantly lower levels of lysophosphatidylcholines, lipid species shown to enhance insulin secretion in ?-cells. Gene expression profiling revealed increased expression of uncoupling protein 2 and genes involved in fatty acid transport and ?-oxidation. In summary, transgenic overexpression of PPAR? in ?-cells in diet-induced obesity negatively impacts whole-animal carbohydrate metabolism associated with altered islet lipid content, increased expression of ?-oxidative genes, and reduced ?-cell mass. PMID:25051434

Hogh, K-Lynn N; Craig, Michael N; Uy, Christopher E; Nygren, Heli; Asadi, Ali; Speck, Madeline; Fraser, Jordie D; Rudecki, Alexander P; Baker, Robert K; Oreši?, Matej; Gray, Sarah L

2014-10-01

107

Unacylated Ghrelin Induces Oxidative Stress Resistance in a Glucose Intolerance and Peripheral Artery Disease Mouse Model by Restoring Endothelial Cell miR-126 Expression.  

PubMed

Reactive oxygen species (ROS) are crucial in long-term diabetes complications, including peripheral artery disease (PAD). In this study, we have investigated the potential clinical impact of unacylated ghrelin (UnAG) in a glucose intolerance and PAD mouse model. We demonstrate that UnAG is able to protect skeletal muscle and endothelial cells (ECs) from ROS imbalance in hind limb ischemia-subjected ob/ob mice. This effect translates into reductions in hind limb functional impairment. We show that UnAG rescues sirtuin 1 (SIRT1) activity and superoxide dismutase-2 (SOD-2) expression in ECs. This leads to SIRT1-mediated p53 and histone 3 lysate 56 deacetylation and results in reduced EC senescence in vivo. We demonstrate, using small interfering RNA technology, that SIRT1 is also crucial for SOD-2 expression. UnAG also renews micro-RNA (miR)-126 expression, resulting in the posttranscriptional regulation of vascular cell adhesion molecule 1 expression and a reduced number of infiltrating inflammatory cells in vivo. Loss-of-function experiments that target miR-126 demonstrate that miR-126 also controls SIRT1 and SOD-2 expression, thus confirming its role in driving UnAG-mediated EC protection against ROS imbalance. These results indicate that UnAG protects vessels from ROS imbalance in ob/ob mice by rescuing miR-126 expression, thus emphasizing its potential clinical impact in avoiding limb loss in PAD. PMID:25368096

Togliatto, Gabriele; Trombetta, Antonella; Dentelli, Patrizia; Gallo, Sara; Rosso, Arturo; Cotogni, Paolo; Granata, Riccarda; Falcioni, Rita; Delale, Thomas; Ghigo, Ezio; Brizzi, Maria Felice

2015-04-01

108

Monoclonal Antibody Targeting of Fibroblast Growth Factor Receptor 1c Ameliorates Obesity and Glucose Intolerance via Central Mechanisms  

PubMed Central

We have generated a novel monoclonal antibody targeting human FGFR1c (R1c mAb) that caused profound body weight and body fat loss in diet-induced obese mice due to decreased food intake (with energy expenditure unaltered), in turn improving glucose control. R1c mAb also caused weight loss in leptin-deficient ob/ob mice, leptin receptor-mutant db/db mice, and in mice lacking either the melanocortin 4 receptor or the melanin-concentrating hormone receptor 1. In addition, R1c mAb did not change hypothalamic mRNA expression levels of Agrp, Cart, Pomc, Npy, Crh, Mch, or Orexin, suggesting that R1c mAb could cause food intake inhibition and body weight loss via other mechanisms in the brain. Interestingly, peripherally administered R1c mAb accumulated in the median eminence, adjacent arcuate nucleus and in the circumventricular organs where it activated the early response gene c-Fos. As a plausible mechanism and coinciding with the initiation of food intake suppression, R1c mAb induced hypothalamic expression levels of the cytokines Monocyte chemoattractant protein 1 and 3 and ERK1/2 and p70 S6 kinase 1 activation. PMID:25427253

Lelliott, Christopher J.; Ahnmark, Andrea; Admyre, Therese; Ahlstedt, Ingela; Irving, Lorraine; Keyes, Feenagh; Patterson, Laurel; Mumphrey, Michael B.; Bjursell, Mikael; Gorman, Tracy; Bohlooly-Y, Mohammad; Buchanan, Andrew; Harrison, Paula; Vaughan, Tristan; Berthoud, Hans-Rudolf; Lindén, Daniel

2014-01-01

109

Relationship of the angiotensin-converting enzyme gene polymorphism to glucose intolerance, insulin resistance, and hypertension in NIDDM  

Microsoft Academic Search

The deletion (D) allele of the angiotensin-converting enzyme (ACE) gene insertion\\/deletion (I\\/D) polymorphism has been shown\\u000a to be associated with cardiovascular and renal diseases in diabetes mellitus, but the mechanism underlying this association\\u000a is not known. In addition, recent studies of the effect of the ACE gene on blood pressure have yielded conflicting results.\\u000a Therefore, we studied the association of

Xiao-Hong Huang; Vappu Rantalaiho; Ole Wirta; Amos Pasternack; Timo Koivula; Timo Hiltunen; Tapio Nikkari; Terho Lehtimäki

1998-01-01

110

Variants of ENPP1 are associated with childhood and adult obesity and increase the risk of glucose intolerance and type 2 diabetes  

PubMed Central

We identified a childhood obesity locus on chromosome 6q16.3-q24.21 that includes 2.4 Mb common to eight genome scans for Type 2 diabetes (T2D) or obesity1-8. Analysis of the ENPP1 (PC-1) gene, a candidate for insulin resistance9,10 in 6,147 subjects revealed association between a three allele risk haplotype (K121Q/IVS20 delT-11/A>G +1044 TGA, QdelTG) and childhood obesity (OR=1.69, p=0.0006), and in adults with morbid or moderate obesity (OR= 1.50, p= 0.006, OR= 1.37, p= 0.02) and also with T2D (OR=1.56, p=0.00002). The Genotype IBD Sharing Test suggested a contribution of this obesity-associated ENPP1 risk haplotype to the observed chromosome 6q linkage with childhood obesity. The haplotype confers a higher risk of glucose intolerance and T2D to obese children and to their parents and associates with increased serum levels of soluble ENPP1 protein in children. Expression of a long ENPP1 mRNA isoform, which includes the obesity-associated A>G +1044 TGA SNP, was found to be specific for pancreatic islet beta-cells, adipocytes and liver. These findings suggest a primary role for several variants of ENPP1 in mediating insulin-resistance, in the development of both obesity and type 2 diabetes, suggesting an underlying molecular mechanism common to both widespread afflictions. PMID:16025115

Meyre, David; Bouatia-Naji, Nabila; Tounian, Agnès; Samson, Chantal; Lecoeur, Cécile; Vatin, Vincent; Ghoussaini, Maya; Wachter, Christophe; Hercberg, Serge; Charpentier, Guillaume; Patsch, Wolfgang; Pattou, François; Charles, Marie-Aline; Tounian, Patrick; Clément, Karine; Jouret, Béatrice; Weill, Jacques; Maddux, Betty A.; Goldfine, Ira D.; Walley, Andrew; Boutin, Philippe; Dina, Christian; Froguel, Philippe

2005-01-01

111

Beneficial Effects of Angiotensin-Converting Enzyme Inhibitor on Renal Function and Glucose Homeostasis in Diabetics with Hypertension  

Microsoft Academic Search

The antihypertensive efficacy of enalapril and its effects on renal function and glucose homeostasis were investigated in 9 hypertensive patients with non-insulin-dependent diabetes mellitus. Enalapril therapy produced a significant fall in blood pressure (BP) (p < 0.05) and a significant increase in renal blood flow (p < 0.05) without a change in glomerular filtration rate. Furthermore, fasting plasma glucose was

Yasuo Ueda; Wataru Aoi; Shiro Yamachika; Takao Shikaya

1990-01-01

112

Allergies and Intolerance  

MedlinePLUS

... and Intolerance The way in which celiac disease, gluten intolerance and wheat allergy are defined means a great deal to ... celiac disease may provide an incorrect diagnosis of gluten intolerance or wheat allergy. Understanding the differences between these conditions can ...

113

The H1-receptor antagonist cetirizine ameliorates high-fat diet-induced glucose intolerance in male C57BL/6 mice, but not diabetes outcome in female non-obese diabetic (NOD) mice.  

PubMed

Abstract Background. It has been proposed that the histamine 1-receptor (H1-receptor) not only promotes allergic reactions, but also modulates innate immunity and autoimmune reactions. In line with this, we have recently reported that the H1-receptor antagonist cetirizine partially counteracts cytokine-induced beta-cell signaling and destruction. Therefore, the aim of this study was to determine whether cetirizine affects diabetes in NOD mice, a model for human type 1 diabetes, and glucose intolerance in high-fat diet C57BL/6 mice, a model for human glucose intolerance. Methods. Female NOD mice were treated with cetirizine in the drinking water (25 mg/kg body weight) from 9 until 30 weeks of age during which precipitation of diabetes was followed. Male C57BL/6 mice were given a high-fat diet from 5 weeks of age. When the mice were 12 weeks of age cetirizine was given for 2 weeks in the drinking water. The effects of cetirizine were analyzed by blood glucose determinations, glucose tolerance tests, and insulin sensitivity tests. Results. Cetirizine did not affect diabetes development in NOD mice. On the other hand, cetirizine treatment for 1 week protected against high-fat diet-induced hyperglycemia. The glucose tolerance after 2 weeks of cetirizine treatment was improved in high-fat diet mice. We observed no effect of cetirizine on the insulin sensitivity of high-fat diet mice. Conclusion. Our results suggest a protective effect of cetirizine against high-fat diet-induced beta-cell dysfunction, but not against autoimmune beta-cell destruction. PMID:25291144

Anvari, Ebrahim; Wang, Xuan; Sandler, Stellan; Welsh, Nils

2015-03-01

114

The H1-receptor antagonist cetirizine ameliorates high-fat diet-induced glucose intolerance in male C57BL/6 mice, but not diabetes outcome in female non-obese diabetic (NOD) mice  

PubMed Central

Background It has been proposed that the histamine 1-receptor (H1-receptor) not only promotes allergic reactions, but also modulates innate immunity and autoimmune reactions. In line with this, we have recently reported that the H1-receptor antagonist cetirizine partially counteracts cytokine-induced beta-cell signaling and destruction. Therefore, the aim of this study was to determine whether cetirizine affects diabetes in NOD mice, a model for human type 1 diabetes, and glucose intolerance in high-fat diet C57BL/6 mice, a model for human glucose intolerance. Methods Female NOD mice were treated with cetirizine in the drinking water (25 mg/kg body weight) from 9 until 30 weeks of age during which precipitation of diabetes was followed. Male C57BL/6 mice were given a high-fat diet from 5 weeks of age. When the mice were 12 weeks of age cetirizine was given for 2 weeks in the drinking water. The effects of cetirizine were analyzed by blood glucose determinations, glucose tolerance tests, and insulin sensitivity tests. Results Cetirizine did not affect diabetes development in NOD mice. On the other hand, cetirizine treatment for 1 week protected against high-fat diet-induced hyperglycemia. The glucose tolerance after 2 weeks of cetirizine treatment was improved in high-fat diet mice. We observed no effect of cetirizine on the insulin sensitivity of high-fat diet mice. Conclusion Our results suggest a protective effect of cetirizine against high-fat diet-induced beta-cell dysfunction, but not against autoimmune beta-cell destruction. PMID:25291144

Anvari, Ebrahim; Wang, Xuan; Sandler, Stellan

2015-01-01

115

Potentiation of insulin secretion and improvement of glucose intolerance by combining a novel G protein-coupled receptor 40 agonist DS-1558 with glucagon-like peptide-1 receptor agonists.  

PubMed

G protein-coupled receptor 40 (GPR40) is a Gq-coupled receptor for free fatty acids predominantly expressed in pancreatic ?-cells. In recent years, GPR40 agonists have been investigated for use as novel therapeutic agents in the treatment of type 2 diabetes. We discovered a novel small molecule GPR40 agonist, (3S)-3-ethoxy-3-(4-{[(1R)-4-(trifluoromethyl)-2,3-dihydro-1H-inden-1-yl]oxy}phenyl)propanoic acid (DS-1558). The GPR40-mediated effects of DS-1558 on glucose-stimulated insulin secretion were evaluated in isolated islets from GPR40 knock-out and wild-type (littermate) mice. The GPR40-mediated effects on glucose tolerance and insulin secretion were also confirmed by an oral glucose tolerance test in these mice. Furthermore, oral administration of DS-1558 (0.03, 0.1 and 0.3mg/kg) significantly and dose-dependently improved hyperglycemia and increased insulin secretion during the oral glucose tolerance test in Zucker fatty rats, the model of insulin resistance and glucose intolerance. Next, we examined the combination effects of DS-1558 with glucagon like peptide-1 (GLP-1). DS-1558 not only increased the glucose-stimulated insulin secretion by GLP-1 but also potentiated the maximum insulinogenic effects of GLP-1 after an intravenous glucose injection in normal Sprague Dawley rats. Furthermore, the glucose lowering effects of exendin-4, a GLP-1 receptor agonist, were markedly potentiated by the DS-1558 (3mg/kg) add-on in diabetic db/db mice during an intraperitoneal glucose tolerance test. In conclusion, our results indicate that add-on GPR40 agonists to GLP-1 related agents might be a potential treatment compared to single administration of these compounds. Therefore the combinations of these agents are a novel therapeutic option for type 2 diabetes. PMID:24858371

Nakashima, Ryutaro; Yano, Tatsuya; Ogawa, Junko; Tanaka, Naomi; Toda, Narihiro; Yoshida, Masao; Takano, Rieko; Inoue, Masahiro; Honda, Takeshi; Kume, Shoen; Matsumoto, Koji

2014-08-15

116

Differentially regulated protein kinase A (PKA) activity in adipose tissue and liver is associated with resistance to diet-induced obesity and glucose intolerance in mice that lack PKA regulatory subunit type II?.  

PubMed

The cAMP-dependent protein kinase A (PKA) signaling system is widely expressed and has a central role in regulating cellular metabolism in all organ systems affected by obesity. PKA has four regulatory (RI?, RII?, RI?, RII?) and four catalytic (C?, C?, C?, Prkx) subunit isoforms that have tissue-specific expression profiles. In mice, knockout (KO) of RII?, the primary PKA regulatory subunit in adipose tissue or knockout of the catalytic subunit C? resulted in a lean phenotype that resists diet-induced obesity and associated metabolic complications. Here we report that the disruption of the ubiquitously expressed PKA RII? subunit in mice (RII?KO) confers resistance to diet-induced obesity, glucose intolerance, and hepatic steatosis. After 2-week high-fat diet exposure, RII?KO mice weighed less than wild-type littermates. Over time this effect was more pronounced in female mice that were also leaner than their wild-type counterparts, regardless of the diet. Decreased intake of a high-fat diet contributed to the attenuated weight gain in RII?KO mice. Additionally, RII? deficiency caused differential regulation of PKA in key metabolic organs: cAMP-stimulated PKA activity was decreased in liver and increased in gonadal adipose tissue. We conclude that RII? represents a potential target for therapeutic interventions in obesity, glucose intolerance, and nonalcoholic fatty liver disease. PMID:24914943

London, Edra; Nesterova, Maria; Sinaii, Ninet; Szarek, Eva; Chanturiya, Tatyana; Mastroyannis, Spyridon A; Gavrilova, Oksana; Stratakis, Constantine A

2014-09-01

117

The influence of physical training on glucose tolerance, insulin sensitivity, and lipid and lipoprotein concentrations in middle-aged hypertriglyceridaemic, carbohydrate intolerant men  

Microsoft Academic Search

Summary  The effects of 9 weeks of moderate intensity exercise training while on a weight-maintaining diet were studied in 19 untrained middle-aged, hypertriglyceridaemic, carbohydrate intolerant men. Initial mean maximum oxygen consumption was low (29.7±1.0 ml-min–1 · kg–1; mean±SEM) and improved (34.2±1.4ml·min–1·kg–1, pp

R. M. Lampman; D. E. Schteingart; J. T. Santinga; P. J. Savage; C. R. Hydrick; D. R. Bassett; W. D. Block

1987-01-01

118

Lactose Intolerance (For Parents)  

MedlinePLUS

... MORE ON THIS TOPIC Calcium and Your Child Digestive System Milk Allergy in Infants About Recipes for Kids ... Teens With Lactose Intolerance Milk Allergy Lactose Intolerance Digestive System Calcium Contact Us Print Additional resources Send to ...

119

Association of coffee consumption and CYP1A2 polymorphism with risk of impaired fasting glucose in hypertensive patients.  

PubMed

Whether and how coffee use influences glucose metabolism is still a matter for debate. We investigated whether baseline coffee consumption is longitudinally associated with risk of impaired fasting glucose in a cohort of 18-to-45 year old subjects screened for stage 1 hypertension and whether CYP1A2 polymorphism modulates this association. A total of 1,180 nondiabetic patients attending 17 hospital centers were included. Seventy-four percent of our subjects drank coffee. Among the coffee drinkers, 87 % drank 1-3 cups/day (moderate drinkers), and 13 % drank over 3 cups/day (heavy drinkers). Genotyping of CYP1A2 SNP was performed by real time PCR in 639 subjects. At the end of a median follow-up of 6.1 years, impaired fasting glucose was found in 24.0 % of the subjects. In a multivariable Cox regression coffee use was a predictor of impaired fasting glucose at study end, with a hazard ratio (HR) of 1.3 (95 % CI 0.97-1.8) in moderate coffee drinkers and of 2.3 (1.5-3.5) in heavy drinkers compared to abstainers. Among the subjects stratified by CYP1A2 genotype, heavy coffee drinkers carriers of the slow *1F allele (59 %) had a higher adjusted risk of impaired fasting glucose (HR 2.8, 95 % CI 1.3-5.9) compared to abstainers whereas this association was of borderline statistical significance among the homozygous for the A allele (HR 1.7, 95 % CI 0.8-3.8). These data show that coffee consumption increases the risk of impaired fasting glucose in hypertension particularly among carriers of the slow CYP1A2 *1F allele. PMID:25595320

Palatini, Paolo; Benetti, Elisabetta; Mos, Lucio; Garavelli, Guido; Mazzer, Adriano; Cozzio, Susanna; Fania, Claudio; Casiglia, Edoardo

2015-03-01

120

Close relationship between strict blood glucose control, including suppression of blood glucose variability, and mortality reduction in acutely ill patients with glucose intolerance investigated by means of a bedside-type artificial pancreas  

Microsoft Academic Search

The purpose of this study was to elucidate the relationship between strict control of blood glucose (BG) and mortality reduction\\u000a with the use of an artificial pancreas (AP). Patients were evaluated in the (1) early phase (E phase: mean 3.3 ± 2.6 days\\u000a after admission, n = 84) and in the (2) late phase (L phase: mean 9.9 ± 3.3 days, n = 88), and were classified into a (1)

Masami HoshinoYoshikura Haraguchi; Yoshikura Haraguchi; Iwanori Mizushima; Motohiro Sakai

2010-01-01

121

Use of Glucose, Insulin, and C-Reactive Protein to Determine Need for Glucose Tolerance Testing  

Microsoft Academic Search

Objective: Glucose intolerance has been shown to be a better predictor of morbidity and mortality than impaired fasting glucose. However, glucose tolerance tests are inconvenient and expensive. This study evaluated the relative frequencies of glucose intolerance and impaired fasting glucose and sought to determine if 2-hour glucose could be predicted from simple demographic and laboratory data in an obese population.Research

Warren G. Thompson; Erik J. Bergstralh; Jeffrey M. Slezak

2003-01-01

122

Hypoxia-induced glucose-6-phosphate dehydrogenase overexpression and -activation in pulmonary artery smooth muscle cells: implication in pulmonary hypertension.  

PubMed

Severe pulmonary hypertension is a debilitating disease with an alarmingly low 5-yr life expectancy. Hypoxia, one of the causes of pulmonary hypertension, elicits constriction and remodeling of the pulmonary arteries. We now know that pulmonary arterial remodeling is a consequence of hyperplasia and hypertrophy of pulmonary artery smooth muscle (PASM), endothelial, myofibroblast, and stem cells. However, our knowledge about the mechanisms that cause these cells to proliferate and hypertrophy in response to hypoxic stimuli is still incomplete, and, hence, the treatment for severe pulmonary arterial hypertension is inadequate. Here we demonstrate that the activity and expression of glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the pentose phosphate pathway, are increased in hypoxic PASM cells and in lungs of chronic hypoxic rats. G6PD overexpression and -activation is stimulated by H2O2. Increased G6PD activity contributes to PASM cell proliferation by increasing Sp1 and hypoxia-inducible factor 1? (HIF-1?), which directs the cells to synthesize less contractile (myocardin and SM22?) and more proliferative (cyclin A and phospho-histone H3) proteins. G6PD inhibition with dehydroepiandrosterone increased myocardin expression in remodeled pulmonary arteries of moderate and severe pulmonary hypertensive rats. These observations suggest that altered glucose metabolism and G6PD overactivation play a key role in switching the PASM cells from the contractile to synthetic phenotype by increasing Sp1 and HIF-1?, which suppresses myocardin, a key cofactor that maintains smooth muscle cell in contractile state, and increasing hypoxia-induced PASM cell growth, and hence contribute to pulmonary arterial remodeling and pathogenesis of pulmonary hypertension. PMID:25480333

Chettimada, Sukrutha; Gupte, Rakhee; Rawat, Dhwajbahadur; Gebb, Sarah A; McMurtry, Ivan F; Gupte, Sachin A

2015-02-01

123

HIS-388, a novel orally active and long-acting 11?-hydroxysteroid dehydrogenase type 1 inhibitor, ameliorates insulin sensitivity and glucose intolerance in diet-induced obesity and nongenetic type 2 diabetic murine models.  

PubMed

11?-Hydroxysteroid dehydrogenase type 1 (11?-HSD1) is considered a potential therapeutic target in the treatment of type 2 diabetes mellitus. In this study, we investigated the pharmacological properties of HIS-388 (N-[(1R,2s,3S,5s,7s)-5-hydroxyadamantan-2-yl]-3-(pyridin-2-yl) isoxazole-4-carboxamide), a newly synthesized 11?-HSD1 inhibitor, using several mouse models. In cortisone pellet-implanted mice in which hypercortisolism and hyperinsulinemia occur, single administration of HIS-388 exhibited potent and prolonged suppression of plasma cortisol and lowered plasma insulin levels. These effects were more potent than those achieved using the same dose of other 11?-HSD1 inhibitors (carbenoxolone and compound 544 [3-[(1s,3s)-adamantan-1-yl]-6,7,8,9-tetrahydro-5H-[1,2,4]triazolo[4,3-a]azepine]), indicating that HIS-388 potently and continuously suppresses 11?-HSD1 enzyme activity in vivo. In diet-induced obese mice, HIS-388 significantly decreased fasting blood glucose, plasma insulin concentration, and homeostasis model assessment-insulin resistance score, and ameliorated insulin sensitivity. In addition, HIS-388 significantly reduced body weight and suppressed the elevation of blood glucose during the pyruvate tolerance test. In nongenetic type 2 diabetic mice with disease induced by a high-fat diet and low-dose streptozotocin, HIS-388 also significantly decreased postprandial blood glucose and plasma insulin levels and improved glucose intolerance. The effects of HIS-388 on glucose metabolism were indistinguishable from those of an insulin sensitizer, pioglitazone. Our results suggest that HIS-388 is a potent agent against type 2 diabetes. Moreover, amelioration of diabetic symptoms by HIS-388 was at least in part attributable to an antiobesity effect or improvement of hepatic insulin resistance. Therefore, potent and long-lasting inhibition of 11?-HSD1 enzyme activity may be an effective approach for the treatment of type 2 diabetes and obesity-associated disease. PMID:25100752

Okazaki, Seiji; Takahashi, Takehiro; Iwamura, Tomokatsu; Nakaki, Junko; Sekiya, Yumiko; Yagi, Mai; Kumagai, Hiroki; Sato, Mikiya; Sakami, Satoshi; Nitta, Aiko; Kawai, Koji; Kainoh, Mie

2014-10-01

124

Hypertension  

MedlinePLUS

... or secondary. Most people with hypertension have the primary form. This type of high blood pressure is caused by high-salt diets, being overweight, ... can cause secondary hypertension may include: Cushing syndrome Primary ... can also cause high blood pressure, as this tricks the kidneys into thinking blood ...

125

[Hypertension].  

PubMed

Hypertension is well known to one of the risk factors to reduce cognitive function, however, it is still unclear whether anti-hypertensive therapy is effective to prevent development of dementia or Alzheimer's disease. Epidemiological studies suggested antihypertensive therapy from the middle-age could reduce risk of dementia. The meta-analysis including HYVET also suggested blood pressure lowering from the elderly might be also effective to prevent development of dementia. The network meta-analysis and the cohort study using mega-data bank suggested ARB might be effective to prevent development of dementia or Alzheimer's disease compared to administration with other anti-hypertensive drugs. Although the further major clinical investigation is required, anti-hypertensive treatment might be useful to manage hypertensive patients with dementia. PMID:24796098

Ohishi, Mitsuru

2014-04-01

126

Chronic inhibition of dipeptidyl peptidase-IV with ASP8497 improved the HbA(1c) level, glucose intolerance, and lipid parameter level in streptozotocin-nicotinamide-induced diabetic mice.  

PubMed

Dipeptidyl peptidase-IV (DPP-IV) is the primary inactivator of glucoregulatory incretin hormones, and DPP-IV inhibitors are expected to become a useful new class of anti-diabetic agent. The aim of the present study is to characterize the chronic in vivo profile of the DPP-IV inhibitor ASP8497. In streptozotocin-nicotinamide-induced diabetic mice, ASP8497 was administered orally for 3 weeks at 1, 3, or 10 mg/kg once daily, which improved the hemoglobin A(1c), non-fasting plasma insulin, fasting blood glucose levels, glucose intolerance, and lipid profiles (plasma triglyceride, non-esterified fatty acid and total cholesterol) with neutral effect on body weight. The pancreatic insulin content and hepatic phosphoenolpyruvate carboxykinase (PEPCK) activity recovered dose-dependently in ASP8497-treated groups. These results revealed that ASP8497 was successful in improving glycemic control and metabolic parameters in streptozotocin-nicotinamide-induced diabetic mice. It is therefore suggested that ASP8497 may be a potential agent for the treatment of type 2 diabetes. PMID:18762913

Matsuyama-Yokono, Akiko; Tahara, Atsuo; Nakano, Ryosuke; Someya, Yuka; Hayakawa, Masahiko; Shibasaki, Masayuki

2009-02-01

127

Hypertension  

PubMed Central

Hypertension is responsible for roughly one-in-six adult deaths annually in the United States and is associated with five of the top nine causes of death.1 Ten trillion dollars is the estimated annual cost worldwide of the direct and indirect effects of hypertension.2,3 In the U.S. alone, costs estimated at almost $74 billion in 2009 placed a huge economic burden on the health care system.4 The prevalence of hypertension increases with advancing age to the point where more than half of people 60 to 69 years of age and at least three-fourths of those 70 years of age and older are affected.5 Most individuals with hypertension do not have it adequately controlled.1,6 Medication noncompliance due to avoidance of side effects is suggested to be a primary factor.6 The epidemic incidence of hypertension and its significant cost to society indicate that a well-tolerated, cost-effective approach to treatment is urgently needed. PMID:24278815

LePine, Todd

2012-01-01

128

Dietary Intake and Serum and Hair Concentrations of Minerals and their Relationship with Serum Lipids and Glucose Levels in Hypertensive and Obese Patients with Insulin Resistance  

Microsoft Academic Search

Inadequate minerals intake, as well as disruption of some metabolic processes in which microelements are cofactors, are suggested\\u000a to lead to the development of hypertension. The role of minerals in the pathogenesis of hypertension still remains to be explained.\\u000a In the present study, we sought to determine associations between serum and hair mineral concentrations and serum lipids and\\u000a glucose levels.

Joanna Suliburska; Pawe? Bogda?ski; Danuta Pupek-Musialik; Zbigniew Krejpcio

2011-01-01

129

Dietary fructose intolerance, fructan intolerance and FODMAPs  

PubMed Central

Dietary intolerances to fructose, fructans and FODMAPs (Fermentable Oligosaccharides, Disaccharides, Monosaccharides And Polyols) are common, yet poorly recognized and managed. Over the last decade, they have come to the forefront because of new knowledge on the mechanisms and treatment of these conditions. Patients with these problems often present with unexplained bloating, belching, distension, gas, abdominal pain or diarrhea. Here, we have examined the most up-to-date research on these food-related intolerances, discussed controversies, and have provided some guidelines for the dietary management of these conditions. Breath testing for carbohydrate intolerance appears to be standardized and essential for the diagnosis and management of these conditions, especially in the Western population. While current research shows that the FODMAP diet may be effective in treating irritable bowel syndrome, additional research is needed to identify more foods items that are high in FODMAPs, and to assess the long-term efficacy and safety of dietary interventions. PMID:24357350

Fedewa, Amy; Rao, Satish S. C.

2014-01-01

130

The effects of antihypertensive drugs on chromium status, glucose metabolism, and antioxidant and inflammatory indices in spontaneously hypertensive rats.  

PubMed

The long-term use of hypotensive drugs may cause side effects, including impaired glucose metabolism and mineral status. This study tested the hypothesis that some hypotensive drugs can affect tissular chromium levels and indices of glucose metabolic and antioxidant potential in rats. The experiment was performed on 40 male spontaneously hypertensive rats (SHRs), which were assigned to five groups: control (C), with perindopril (PR), with metoprolol (MT), with indapamide (ID), and with amlodipine (AM). All rats were provided ad libitum standard diet (with or without drugs) and distilled water for 45 days. Glucose and insulin levels, along with total antioxidant status (TAS) and concentrations of TNF-alpha and C-reactive protein, were assayed in serum. Chromium concentrations in the liver and kidney were determined using the flame atomic absorption spectrometry method. Detailed statistical analysis was performed using Statistica for Windows 10.0 (StatSoft, Poland). One-way analysis of variance (ANOVA), followed by a post hoc Tukey test, was used to compare the data between groups. Treatment with indapamide and amlodipine resulted in significantly higher chromium concentrations in the liver and kidney (AM) of the rats, compared with the control group. A markedly higher concentration of glucose was found in the ID group. Treatment with amlodipine significantly increased TAS levels in serum and decreased TNF-alpha concentration in serum of the rats. A significant positive correlation between chromium concentration in tissues and serum TAS level was observed, as was a significant negative correlation between chromium concentration in the kidneys, and TNF-alpha and glucose levels in serum. In conclusion, the administration of amlodipine may lead to an increase in chromium accumulation in the internal organs, which is associated with increased antioxidant status and suppression of the inflammatory response of cells in SHRs. PMID:24249586

Suliburska, Joanna; Krejpcio, Zbigniew; Staniek, Halina; Król, Ewelina; Bogdanski, Pawel; Kupsz, Justyna; Hertig, Iwona

2014-01-01

131

Synergistic effect of uricase blockade plus physiological amounts of fructose-glucose on glomerular hypertension and oxidative stress in rats  

PubMed Central

Fructose in sweetened beverages (SB) increases the risk for metabolic and cardiorenal disorders, and these effects are in part mediated by a secondary increment in uric acid (UA). Rodents have an active uricase, thus requiring large doses of fructose to increase plasma UA and to induce metabolic syndrome and renal hemodynamic changes. We therefore hypothesized that the effects of fructose in rats might be enhanced in the setting of uricase inhibition. Four groups of male Sprague-Dawley rats (n = 7/group) were studied during 8 wk: water + vehicle (V), water + oxonic acid (OA; 750 mg/k BW), sweetened beverage (SB; 11% fructose-glucose combination) + V, and SB + OA. Systemic blood pressure, plasma UA, triglycerides (TG), glucose and insulin, glomerular hemodynamics, renal structural damage, renal cortex and liver UA, TG, markers of oxidative stress, mitDNA, fructokinase, and fatty liver synthase protein expressions were evaluated at the end of the experiment. Chronic hyperuricemia and SB induced features of the metabolic syndrome, including hypertension, hyperuricemia, hyperglycemia, and systemic and hepatic TG accumulation. OA alone also induced glomerular hypertension, and SB alone induced insulin resistance. SB + OA induced a combined phenotype including metabolic and renal alterations induced by SB or OA alone and in addition also acted synergistically on systemic and glomerular pressure, plasma glucose, hepatic TG, and oxidative stress. These findings explain why high concentrations of fructose are required to induce greater metabolic changes and renal disease in rats whereas humans, who lack uricase, appear to be much more sensitive to the effects of fructose. PMID:23303409

Tapia, Edilia; Cristóbal, Magdalena; García-Arroyo, Fernando E.; Soto, Virgilia; Monroy-Sánchez, Fabiola; Pacheco, Ursino; Lanaspa, Miguel A.; Roncal-Jiménez, Carlos A.; Cruz-Robles, David; Ishimoto, Takuji; Madero, Magdalena; Johnson, Richard J.

2013-01-01

132

What Causes Lactose Intolerance?  

MedlinePLUS

... describe why a person may not have enough lactase 1 : Primary lactose intolerance . This type develops in people who were once ... such as from severe illness or disease. Congenital lactose intolerance . Infants born with this rare type make no lactase at all. It is not uncommon for secondary ...

133

Aortic Pulse-Wave Velocity and Its Relationship to Mortality in Diabetes and Glucose Intolerance An Integrated Index of Vascular Function?  

Microsoft Academic Search

Background—Arterial distensibility measures, generally from pulse-wave velocity (PWV), are widely used with little knowledge of relationships to patient outcome. We tested whether aortic PWV predicts cardiovascular and all-cause mortality in type 2 diabetes and glucose-tolerance-tested (GTT) multiethnic population samples. Methods and Results—Participants were randomly sampled from (1) a type 2 diabetes outpatient clinic and (2) primary care population registers, from

Kennedy Cruickshank; Lisa Riste; Simon G. Anderson; John S. Wright; Graham Dunn; Ray G. Gosling

134

Glucan-rich polysaccharides from Pleurotus sajor-caju (Fr.) Singer prevents glucose intolerance, insulin resistance and inflammation in C57BL/6J mice fed a high-fat diet  

PubMed Central

Background Pleurotus sajor-caju (P. sajor-caju) has been extremely useful in the prevention of diabetes mellitus due to its low fat and high soluble fiber content for thousands of years. Insulin resistance is a key component in the development of diabetes mellitus which is caused by inflammation. In this study, we aimed to investigate the in vivo efficacy of glucan-rich polysaccharide of P. sajor-caju (GE) against diabetes mellitus and inflammation in C57BL/6J mice fed a high-fat diet. Methods Diabetes was induced in C57BL/6J mice by feeding a high-fat diet. The mice were randomly assigned to 7 groups (n=6 per group). The control groups in this study were ND (for normal diet) and HFD (for high-fat diet). The treated groups were ND240 (for normal diet) (240 mg/kg b.w) and HFD60, HFD120 and HFD240 (for high-fat), where the mice were administrated with three dosages of GE (60, 120, 240 mg GE/kg b.w respectively). Metformin (2 mg/kg b.w) served as positive control. The glucose tolerance test, glucose and insulin levels were measured at the end of 16 weeks. Expressions of genes for inflammatory markers, GLUT-4 and adiponectin in the adipose tissue of the mice were assessed. One-way ANOVA and Duncan’s multiple range tests (DMRT) were used to determine the significant differences between groups. Results GE treated groups improved the glucose tolerance, attenuated hyperglycemia and hyperinsulinemia in the mice by up-regulating the adiponectin and GLUT-4 gene expressions. The mice in GE treated groups did not develop insulin resistance. GE also down-regulated the expression of inflammatory markers (IL-6, TNF-?, SAA2, CRP and MCP-1) via attenuation of nuclear transcription factors (NF-?B). Conclusion Glucan-rich polysaccharide of P. sajor-caju can serve as a potential agent for prevention of glucose intolerance, insulin resistance and inflammation. PMID:23259700

2012-01-01

135

Effect of angiotensin receptor blockade on insulin sensitivity and endothelial function in abdominally obese hypertensive patients with impaired fasting glucose.  

PubMed

AngII (angiotensin II) may contribute to cardiovascular risk in obesity via adverse effects on insulin sensitivity and endothelial function. In the present study, we examined the effects of ARB (angiotensin receptor blocker) therapy (losartan, 100 mg/day) on insulin sensitivity and endothelial function in 53 subjects with stage I hypertension, abdominal obesity and impaired fasting glucose. The study design was a randomized double-blinded parallel design placebo-controlled multi-centre trial of 8 weeks duration. We used the hyperinsulinaemic-euglycaemic clamp technique to measure insulin sensitivity (expressed as the 'M/I' value) and RH-PAT (reactive hyperaemia-peripheral arterial tonometry) to measure endothelial function. Additional measures included HOMA (homoeostasis model assessment)-B, an index of pancreatic ?-cell function, and markers of inflammation [e.g. CRP (C-reactive protein)] and oxidative stress (e.g. F2-isoprostanes). ARB therapy did not alter insulin sensitivity [5.2 (2.7) pre-treatment and 4.6 (1.6) post-treatment] compared with placebo therapy [6.1 (2.9) pre-treatment and 5.3 (2.7) post-treatment; P value not significant], but did improve the HOMA-B compared with placebo therapy (P=0.05). ARB therapy also did not change endothelial function [RH-PAT, 2.15 (0.7) pre-treatment and 2.11 (0.7) post-treatment] compared with placebo therapy [RH-PAT, 1.81 (0.5) pre-treatment and 1.76 (0.7) post-treatment; P value not significant]. Markers of inflammation and oxidative stress were not significantly changed by ARB therapy. In conclusion, ARB therapy did not alter peripheral insulin sensitivity or endothelial function in this cohort of patients with essential hypertension, abdominal obesity and impaired fasting glucose, but did improve pancreatic ?-cell function. PMID:21861845

Perlstein, Todd S; Henry, Robert R; Mather, Kieren J; Rickels, Michael R; Abate, Nicola I; Grundy, Scott M; Mai, Yabing; Albu, Jeanine B; Marks, Jennifer B; Pool, James L; Creager, Mark A

2012-02-01

136

Relation of blood volume and blood pressure in orthostatic intolerance  

NASA Technical Reports Server (NTRS)

A complex but crucial relationship exists between blood volume and blood pressure in human subjects; it has been recognized that in essential hypertension, renovascular hypertension, and pheochromocytoma, the relationship between plasma volume and diastolic blood pressure is an inverse one. This phenomenon has not been studied in individuals with low normal and reduced blood pressures. Orthostatic intolerance is a commonly encountered abnormality in blood pressure regulation often associated with tachycardia in the standing position. Most of these patients have varying degrees of reduced blood volume. We tested the hypothesis that the relationship previously found between plasma volume and diastolic blood pressure in pressor states would also hold in orthostatic intolerance. We studied 16 patients with a history of symptomatic orthostatic intolerance associated with an elevation in plasma norepinephrine in the upright posture and hypovolemia in 9 patients and normovolemia in 7 patients. Our studies demonstrate an inverse relationship between plasma volume and diastolic blood pressure in patients with orthostatic intolerance. This finding also holds for the change in diastolic blood pressure in response to upright posture. In this relationship, patients with orthostatic intolerance with high plasma norepinephrine resemble those with essential hypertension, renovascular hypertension, and pheochromocytoma. We conclude that in a variety of conditions at both ends of the blood pressure spectrum, the seemingly paradoxical association of hypovolemia and diastolic blood pressure is preserved.

Jacob, G.; Biaggioni, I.; Mosqueda-Garcia, R.; Robertson, R. M.; Robertson, D.

1998-01-01

137

Intolerance, Prejudice and Discrimination  

E-print Network

Intolerance, Prejudice and Discrimination A European Report Forum Berlin Andreas Zick, Beate Küpper .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 1 Multicultural Europe between Tolerance and Prejudice: General Observations and Project Design 15 1.1 Outsiders in Europe ­ the Targets of Prejudice . . . . . . . . . . . . . . . . . . . . . . . 19

Moeller, Ralf

138

Hereditary fructose intolerance  

MedlinePLUS

Fructosemia; Fructose intolerance; Fructose aldolase B-deficiency; Fructose 1, 6 bisphosphate aldolase deficiency ... B. This substance is needed to break down fructose. If a person without this substance eats fructose ...

139

Study of the effect of changing glucose, insulin, and insulin-like growth factor-I levels on serum corticosteroid binding globulin in lean, obese, and obese subjects with glucose intolerance  

Microsoft Academic Search

We have previously described that serum corticosteroid binding globulin (CBG) concentrations are associated with insulin secretion. The present study was designed to evaluate the effects of changing insulin concentrations, both endogenous and after exogenous insulin administration, on circulating CBG levels in vivo. Serum CBG concentrations were measured during an insulin-modified frequently sampled intravenous (IV) glucose tolerance test (FSIVGT) in 14

Michel Pugeat; Wifredo Ricart

2001-01-01

140

Ethanol extract of the Prunus mume fruits stimulates glucose uptake by regulating PPAR-? in C2C12 myotubes and ameliorates glucose intolerance and fat accumulation in mice fed a high-fat diet.  

PubMed

In this study, we performed in vitro and in vivo studies to examine whether a 70% ethanol extract of Prunus mume fruits (EMS) exhibits anti-diabetic effects. Treatment with EMS increased glucose uptake in C2C12 myotubes, and also increased PPAR-? activity or PPAR-? mRNA expression. To confirm these in vitro results, we next conducted an animal experiment. A high-fat diet significantly increased the body weight, fat accumulation, and glucose levels in mice. Under the same conditions, 5% EMS attenuated the high-fat diet-induced increase in body weight and fat accumulation and improved the impaired fasting glucose level and glucose tolerance. High performance liquid chromatography analysis demonstrated that EMS contained chlorogenic acid, caffeic acid, rutin, luteolin-7-glucoside, naringin, apigenin-7-glucoside, and hesperidin. Taken together, these findings suggest that EMS exerts an anti-diabetic effect both in vitro and in vivo, which is mediated, at least in part, by the activation of PPAR-?. PMID:23993593

Shin, Eun Ju; Hur, Haeng Jeon; Sung, Mi Jeong; Park, Jae Ho; Yang, Hye Jeong; Kim, Myung Sunny; Kwon, Dae Young; Hwang, Jin-Taek

2013-12-15

141

Determining the amounts of urea and glucose in urine of patients with renal complications from diabetes mellitus and hypertension by near-infrared Raman spectroscopy  

NASA Astrophysics Data System (ADS)

Diabetes mellitus and hypertension diseases are frequently found in the same patient, which if untreated predispose to atherosclerotic and kidney diseases. The objective of this study was to identify potential biomarkers in the urine of diabetic and hypertensive patients through dispersive near-infrared Raman spectroscopy. Urine samples were collected from patients with diabetes and hypertension but no complications (LG), high degree of complications (HG), and control ones: one fraction was submitted to biochemical tests and another one was stored frozen (-20°C) until spectral analysis. Samples were warmed up and placed in an aluminum sample holder for Raman spectra collection using a dispersive spectrometer (830 nm wavelength, 300 mW laser power and 20 s exposure time). Spectra were then submitted to Principal Components Analysis. The PCA loading vectors 1 and 3 revealed spectral features of urea/creatinine and glucose, respectively; the PCA scores showed that patients with diabetes/hypertension (LG and HG) had higher amount of glucose in the urine compared to the normal group (p < 0.05), which can bring serious consequences to patients. Also, the PCA scores showed that the amount of urea decreased in the groups with diabetes/hypertension (p < 0.05), which generates the same concern as it is a marker that has a strong importance in the metabolic changes induced by such diseases. These results, applied to the analysis of urine of patients with diabetes/hypertension, can lead to early diagnostic information of complications and a possible disease prognosis in the patients where no complications from diabetes and hypertension were found.

Bispo, Jeyse A. M.; Silveira, Landulfo; Vieira, Elzo E. d. S.; Fernandes, Adriana B.

2013-02-01

142

Orthostatic intolerance: a disorder of young women  

NASA Technical Reports Server (NTRS)

Orthostatic intolerance (OI) is a cause of significant disability in otherwise healthy women seen by gynecologists. Orthostatic tachycardia is often the most obvious hemodynamic abnormality found in OI patients, but symptoms may include dizziness, visual changes, discomfort in the head or neck, poor concentration, fatigue, palpitations, tremulousness, anxiety, and, in some cases, fainting (syncope). It is the most common disorder of blood pressure regulation after essential hypertension, and patients with OI are traditionally women of childbearing age. Estimates suggest that at least 500,000 Americans suffer from some form of OI, and such patients comprise the largest group referred to centers specialized in autonomic disorders. This article reviews recent advances made in the understanding of this condition, potential pathophysiological mechanisms contributing to orthostatic intolerance, and therapeutic alternatives currently available for the management of these patients.

Ali, Y. S.; Daamen, N.; Jacob, G.; Jordan, J.; Shannon, J. R.; Biaggioni, I.; Robertson, D.

2000-01-01

143

Beneficial effects of L- and N-type calcium channel blocker on glucose and lipid metabolism and renal function in patients with hypertension and type II diabetes mellitus.  

PubMed

It has been proved that cilnidipine has N-type calcium channels inhibitory activity as well as L-type calcium channels and inhibits excessive release of norepinephrine from the sympathetic nerve ending. This study was undertaken to compare the efficacy of amlodipine (an inhibitor of L-type calcium channels) and cilnidipine (an inhibitor of both L-type and N-type calcium channels) in patients with hypertension and type II diabetes mellitus. Seventy-seven hypertensive patients were divided into two groups according to presence/absence of type II diabetes mellitus. In these two groups of patients, the effects of amlodipine and cilnidipine on glucose and lipid metabolism and renal function were compared. As for glucose and lipid metabolism, homeostasis model assessment insulin resistance (HOMA-R) level in the non-diabetic group and triglyceride in the diabetes group were significantly lower with cilnidipine than with amlodipine. As regards renal function in the diabetic group, estimated glomerular filtration rate (eGFR) was significantly higher and urinary albumin/creatinine ratio was significantly lower with cilnidipine than with amlodipine. Cilnidipine which inhibits N-type calcium channels is more useful for patients with hypertension and diabetes mellitus from its effects on glucose and lipid metabolism and renal function. PMID:20337636

Masuda, Takashi; Ogura, Misao N; Moriya, Tatsumi; Takahira, Naonobu; Matsumoto, Takuya; Kutsuna, Toshiki; Hara, Miyako; Aiba, Naoko; Noda, Chiharu; Izumi, Tohru

2011-02-01

144

Sorbitol intolerance in adults.  

PubMed

Sorbitol is a commonly used sugar substitute in "sugar-free" food products. Although sorbitol intolerance manifested by abdominal pain, bloating, and diarrhea has been observed in children, it has not been well documented in adults. Forty-two healthy adults (23 whites, 19 nonwhites) participated in this study. After ingestion of 10 g of sorbitol solution, end expiratory breath samples were collected at 15-min intervals for 4 h and analyzed for H2 concentration. Clinical sorbitol intolerance was detected in 43% of the whites and 55% of the nonwhites, the difference not being statistically significant. However, severe clinical sorbitol intolerance was significantly more prevalent in nonwhites (32%) as compared to whites (4%). There was a good correlation between the severity of symptoms and the amount of hydrogen exhaled. Dietetic foods, many of them containing sorbitol, are very popular with diabetics and "weight watchers." Based on our observations, we believe that a large number of adults could be suffering from sorbitol-induced nonspecific abdominal symptoms and diarrhea. These symptoms could lead to an extensive diagnostic work-up and lifelong diagnosis of irritable bowel syndrome. PMID:4036946

Jain, N K; Rosenberg, D B; Ulahannan, M J; Glasser, M J; Pitchumoni, C S

1985-09-01

145

Is It Food Allergy or Food Intolerance?  

MedlinePLUS

... this page: Lactose intolerance Food additives Gluten intolerance Food poisoning Histamine toxicity Other conditions Lactose intolerance Lactose is ... not considered a food allergy. back to top Food poisoning Some of the symptoms of food allergy, such ...

146

Association of an Abnormal Blood Glucose Level and Morning Blood Pressure Surge in Elderly Subjects With Hypertension  

Microsoft Academic Search

BackgroundWe previously reported that morning blood pressure (BP) surge (MBPS) was an independent risk factor for stroke. We evaluated the determinants of MBPS in hypertensive patients.MethodsWe analyzed 24-h ambulatory BP monitoring (ABPM) records in 458 hypertensive patients (mean: 72.2 ± 8.5 years). The MBPS was calculated as the mean systolic BP (SBP) over 2 h after waking minus mean SBP

Motohiro Shimizu; Joji Ishikawa; Kazuo Eguchi; Satoshi Hoshide; Kazuyuki Shimada; Kazuomi Kario

2009-01-01

147

Pulmonary hypertension  

MedlinePLUS

Pulmonary arterial hypertension; Sporadic primary pulmonary hypertension; Familial primary pulmonary hypertension; Idiopathic pulmonary arterial hypertension; Primary pulmonary hypertension; PPH; Secondary pulmonary hypertension

148

Lactose intolerance in Thai adults.  

PubMed

Lactose intolerance is common in Thai adults who ingest cow's milk but its incidence has not been clearly defined The authors evaluated 45 volunteers (15 males, 35 females), aged 21-31 yrs old, who drank one 240-ml box of milk daily. A Lactose tolerance test was performed using a breath-hydrogen test (BHT) after oral intake of 25 g of lactose dissolved in 250 ml of water The presence of gastrointestinal symptoms of lactose intolerance, flatulence, abdominal pain and diarrhea, were recorded Twenty-one subjects (47%) were categorized as lactose malabsorbers and intolerant, two subjects (4%) were malabsorbers but tolerant, and 22 of 45 (49%) were absorbers and tolerant. The incidence of lactose malabsorption was, thus, 51%; symptoms of intolerance were found in 21 of the 23 malabsorbers, making the incidence of lactose intolerance 47%. In the lactose malabsorbant and intolerant group, the more breath-hydrogen (H) the more symptoms observed All subjects who had a negative breath-H2 test had no symptoms. The breath-H2 test should be used as a standard method to evaluate lactose absorption and lactose tolerance. The incidence of lactose intolerance has decreased from the past and the symptoms are not so severe that the people limit the consumption of milk since it is a major source of food containing good quality of protein and calcium. PMID:15822548

Densupsoontorn, Narumon; Jirapinyo, Pipop; Thamonsiri, Nuchnoi; Chantaratin, Sasitorn; Wongarn, Renu

2004-12-01

149

How Is Lactose Intolerance Managed?  

MedlinePLUS

... Information Clinical Trials Resources and Publications How is lactose intolerance managed? Skip sharing on social media links Share this: Page Content No treatment can change the body's ability to make lactase. 1 But most people who have problems digesting ...

150

Genetics Home Reference: Lactose intolerance  

MedlinePLUS

... Patients and Families Resources for Health Professionals What glossary definitions help with understanding lactose intolerance? autosomal ; autosomal ... many other terms in the Genetics Home Reference Glossary . See also Understanding Medical Terminology . References (9 links) ...

151

How Is Lactose Intolerance Diagnosed?  

MedlinePLUS

... following tests also can help diagnose lactose intolerance: Hydrogen breath test. For this test, a person drinks ... beverage that has lactose in it. Then, the hydrogen level in the breath is measured at set ...

152

Model-based assessment of insulin sensitivity of glucose disposal and endogenous glucose production from double-tracer oral glucose tolerance test  

Microsoft Academic Search

A new mathematical model of short-term glucose regulation by insulin is proposed to exploit the oral glucose tolerance test (OGTT), which is commonly used for clinical diagnosis of glucose intolerance and diabetes. Contributions of endogenous and exogenous sources to measured plasma glucose concentrations have been separated by means of additional oral administration and constant intravenous infusion of glucose labeled with

Karl Thomaseth; Alessandra Pavan; Rachele Berria; Leonard Glass; Ralph Defronzo; Amalia Gastaldelli

2008-01-01

153

Hereditary fructose intolerance.  

PubMed Central

Hereditary fructose intolerance (HFI, OMIM 22960), caused by catalytic deficiency of aldolase B (fructose-1,6-bisphosphate aldolase, EC 4.1.2.13), is a recessively inherited condition in which affected homozygotes develop hypoglycaemic and severe abdominal symptoms after taking foods containing fructose and cognate sugars. Continued ingestion of noxious sugars leads to hepatic and renal injury and growth retardation; parenteral administration of fructose or sorbitol may be fatal. Direct detection of a few mutations in the human aldolase B gene on chromosome 9q facilitates the genetic diagnosis of HFI in many symptomatic patients. The severity of the disease phenotype appears to be independent of the nature of the aldolase B gene mutations so far identified. It appears that hitherto there has been little, if any, selection against mutant aldolase B alleles in the population: in the UK, approximately 1.3% of neonates harbour one copy of the prevalent A149P disease allele. The ascendance of sugar as a major dietary nutrient, especially in western societies, may account for the increasing recognition of HFI as a nutritional disease and has shown the prevalence of mutant aldolase B genes in the general population. The severity of clinical expression correlates well with the immediate nutritional environment, age, culture, and eating habits of affected subjects. Here we review the biochemical, genetic, and molecular basis of human aldolase B deficiency in HFI, a disorder which responds to dietary therapy and in which the principal manifestations of disease are thus preventable. Images PMID:9610797

Ali, M; Rellos, P; Cox, T M

1998-01-01

154

Chronic inhibition of 11 ? -hydroxysteroid dehydrogenase type 1 activity decreases hypertension, insulin resistance, and hypertriglyceridemia in metabolic syndrome.  

PubMed

Metabolic syndrome is a constellation of risk factors including hypertension, dyslipidemia, insulin resistance, and obesity that promote the development of cardiovascular disease. Metabolic syndrome has been associated with changes in the secretion or metabolism of glucocorticoids, which have important functions in adipose, liver, kidney, and vasculature. Tissue concentrations of the active glucocorticoid cortisol are controlled by the conversion of cortisone to cortisol by 11 ? -hydroxysteroid dehydrogenase type 1 (11 ? -HSD1). Because of the various cardiovascular and metabolic activities of glucocorticoids, we tested the hypothesis that 11 ? -HSD1 is a common mechanism in the hypertension, dyslipidemia, and insulin resistance in metabolic syndrome. In obese and lean SHR/NDmcr-cp (SHR-cp), cardiovascular, metabolic, and renal functions were measured before and during four weeks of administration of vehicle or compound 11 (10 mg/kg/d), a selective inhibitor of 11 ? -HSD1. Compound 11 significantly decreased 11 ? -HSD1 activity in adipose tissue and liver of SHR-cp. In obese SHR-cp, compound 11 significantly decreased mean arterial pressure, glucose intolerance, insulin resistance, hypertriglyceridemia, and plasma renin activity with no effect on heart rate, body weight gain, or microalbuminuria. These results suggest that 11 ? -HSD1 activity in liver and adipose tissue is a common mediator of hypertension, hypertriglyceridemia, glucose intolerance, and insulin resistance in metabolic syndrome. PMID:23586038

Schnackenberg, Christine G; Costell, Melissa H; Krosky, Daniel J; Cui, Jianqi; Wu, Charlene W; Hong, Victor S; Harpel, Mark R; Willette, Robert N; Yue, Tian-Li

2013-01-01

155

Contribution of glomerular filtration rate to 10-year cardiovascular and mortality risk among hypertensive adults: Tehran lipid and glucose study.  

PubMed

The authors tested the hypotheses that (1) estimated glomerular filtration rate (eGFR) predicts cardiovascular disease (CVD) or mortality risk among hypertensive patients, (2) associations are curvilinear, and (3) diabetes modifies these associations. Data from a 10-year follow-up of 3179 hypertensive patients 18 years and older were analyzed. Measurements included eGFR and CVD risk factors, and outcomes were CVD and mortality. Cox models were developed to estimate the hazard ratios (HRs) for different endpoints for a 1-standard deviation (SD) increment in eGFR. The nonlinearity in associations was examined by cubic spline method. Mean (SD) age of the participants (59.0% women) was 56.3 (12.3) years. During follow-up (10-year), 629 incident cases of CVD (296 women) and 320 deaths (130 women) were documented. The incidence rate of different outcomes decreased across increasing eGFR quintiles. Among men, irrespective of their diabetes status, eGFR was inversely associated with risk of mortality. Among women, irrespective of their diabetes status, eGFR did not predict mortality. Neither among men nor among women did eGFR predict CVD or coronary heart disease. No evidence was found for nonlinearity in these associations. eGFR was independently associated with mortality among hypertensive men with or without diabetes. When information on traditional CVD risk factors was available, eGFR provided no additional predictive value for CVD. PMID:23614851

Mohebi, Reza; Bozorgmanesh, Mohammadreza; Sheikholeslami, Farhad; Azizi, Fereidoun; Hadaegh, Farzad

2013-05-01

156

Overcoming the barrier of lactose intolerance to reduce health disparities.  

PubMed Central

Federal health goals for the public have focused on reducing health disparities that exist between whites and various racial and ethnic groups. Many of the chronic diseases for which African Americans are at greater risk- hypertension, stroke, colon cancer, and obesity-may be exacerbated by a low intake of calcium and/or other dairy-related nutrients. For example, a low intake of dairy food nutrients, such as calcium, potassium, and magnesium, may contribute to the high risk of hypertension seen in African Americans. The Dietary Approaches to Stop Hypertension (DASH) study demonstrated that a low-fat diet rich in fruits and vegetables (8 to 10 servings) and low-fat dairy foods (3 servings) significantly reduced blood pressure-and was twice as effective in African-American participants. Calcium and dairy food consumption is particularly low among African-American, Hispanic, and Asian populations. Average intakes are near the threshold of 600 to 700 mg/day, below which bone loss and hypertension can result. Although lactose intolerance may be partly to blame for the low calcium intakes due to reduced dairy food consumption by minority populations, culturally determined food preferences and dietary practices learned early in life also play a role. The high incidence figures for primary lactose maldigestion among minority groups grossly overestimates the number who will experience intolerance symptoms after drinking a glass of milk with a meal. Randomized, double-blind, controlled clinical trials have demonstrated that by using a few simple dietary strategies, those who maldigest lactose (have low levels of the lactase enzyme) can easily tolerate a dairy-rich diet that meets calcium intake recommendations. Physicians and other health professionals can help their minority patients and the general public understand how to improve calcium nutrition by overcoming the surmountable barrier of lactose intolerance. At the same time they will be helping to reduce the incidence of calcium-related chronic diseases for which minority populations are at high risk. PMID:11853047

Jarvis, Judith K.; Miller, Gregory D.

2002-01-01

157

Fasting glucose and HbA1c levels as risk factors for the development of hypertension in Japanese individuals: Toranomon hospital health management center study 16 (TOPICS 16).  

PubMed

We investigated the effect of elevated concentrations of fasting plasma glucose (FPG) or hemoglobin A1c (HbA1c) on the risk of development of hypertension among apparently healthy Japanese. Studied were 9584 individuals without known diabetes and hypertension. During a 5-year follow-up period, 1098 individuals developed hypertension. Elevated concentrations of FPG, rather than of HbA1c, were significantly predictive of future hypertension. Compared with the lowest quartile category of FPG (<4.9?mmol?l(-1)), the second (4.9-<5.2?mmol?l(-1)), third (5.2-<5.6?mmol?l(-1)) and highest (??5.6?mmol?l(-1)) quartile categories had age-, sex- and body mass index-adjusted odds ratios (95% confidence interval) of 1.35 (1.10, 1.66), 1.39 (1.13, 1.71) and 1.85 (1.51, 2.28) for hypertension, respectively. In the highest quartile of FPG, the multivariate-adjusted OR was 1.37 (1.10, 1.70) compared with the lowest quartile. Results of these adjusted models showed no significant association across quartile categories of HbA1c concentrations and an increased risk of developing hypertension. The joint effect of hyperglycemia and overweight, older age or prehypertension resulted in further elevated ORs for hypertension than the absence of such an association. Higher FPG levels rather than HbA1c were strongly predictive of future hypertension among Japanese. Hyperglycemia along with older age, overweight and prehypertension contributed to identifying individuals at increased risk of developing hypertension. PMID:25231510

Heianza, Y; Arase, Y; Kodama, S; Hsieh, S D; Tsuji, H; Saito, K; Hara, S; Sone, H

2015-04-01

158

Lactose Intolerance: A Guide for Teens  

MedlinePLUS

... without having symptoms. Are there different “types” of lactose intolerance? Yes. Some people are born without the ability to make the enzyme lactase. People with this type of lactose intolerance have ...

159

Colonic fermentation may play a role in lactose intolerance in humans.  

PubMed

The results of our previous study suggested that in addition to the small intestinal lactase activity and transit time, colonic processing of lactose may play a role in lactose intolerance. We investigated whether colonic fermentation of lactose is correlated with lactose intolerance. After 28 Chinese subjects had undergone 1 glucose (placebo) and 2 lactose challenges, consistent lactose tolerant (n = 7) and intolerant (n = 5) subjects with no complaints after glucose administration were classified on the basis of the 6-h symptom scores. Before the challenges, fecal samples were collected for in vitro incubation with lactose. The incubation was carried out in a static system under anaerobic conditions for 5 h during which samples were taken for measurement of short-chain fatty acids, lactate, lactose, glucose, and galactose. Fecal bacterial composition was determined by fluorescent in situ hybridization. The tolerant and intolerant groups did not differ in the rate or degree of hydrolysis of lactose or production of glucose and galactose. The intolerant group produced d- and l-lactate, acetate, propionate, and butyrate significantly faster than the tolerant group. In the intolerant group, the amounts of acetate, propionate, butyrate, and l-lactate produced were higher than those in the tolerant group. Fecal bacterial composition did not differ between the 2 groups. The results indicate that the degree and rate of lactose hydrolysis in the colon do not play a role in lactose intolerance. However, after lactose is hydrolyzed, a faster and higher production of microbial intermediate and end metabolites may be related to the occurrence of symptoms. PMID:16365059

He, Tao; Priebe, Marion G; Harmsen, Hermie J M; Stellaard, Frans; Sun, Xiaohong; Welling, Gjalt W; Vonk, Roel J

2006-01-01

160

Fasting 2-Deoxy-2-[18F]fluoro-d-glucose Positron Emission Tomography to Detect Metabolic Changes in Pulmonary Arterial Hypertension Hearts over 1 Year  

PubMed Central

Background: The development of tools to monitor the right ventricle in pulmonary arterial hypertension (PAH) is of clinical importance. PAH is associated with pathologic expression of the transcription factor hypoxia-inducible factor (HIF)-1?, which induces glycolytic metabolism and mobilization of proangiogenic progenitor (CD34+CD133+) cells. We hypothesized that PAH cardiac myocytes have a HIF-related switch to glycolytic metabolism that can be detected with fasting 2-deoxy-2-[18F]fluoro-d-glucose positron emission tomography (FDG-PET) and that glucose uptake is informative for cardiac function. Methods: Six healthy control subjects and 14 patients with PAH underwent fasting FDG-PET and echocardiogram. Blood CD34+CD133+ cells and erythropoietin were measured as indicators of HIF activation. Twelve subjects in the PAH cohort underwent repeat studies 1 year later to determine if changes in FDG uptake were related to changes in echocardiographic parameters or to measures of HIF activation. Measurements and Results: FDG uptake in the right ventricle was higher in patients with PAH than in healthy control subjects and correlated with echocardiographic measures of cardiac dysfunction and circulating CD34+CD133+ cells but not erythropoietin. Among patients with PAH, FDG uptake was lower in those receiving ?-adrenergic receptor blockers. Changes in FDG uptake over time were related to changes in echocardiographic parameters and CD34+CD133+ cell numbers. Immunohistochemistry of explanted PAH hearts of patients undergoing transplantation revealed that HIF-1? was present in myocyte nuclei but was weakly detectable in control hearts. Conclusions: PAH hearts have pathologic glycolytic metabolism that is quantitatively related to cardiac dysfunction over time, suggesting that metabolic imaging may be useful in therapeutic monitoring of patients. PMID:23509326

Lundgrin, Erika L.; Park, Margaret M.; Sharp, Jacqueline; Tang, W.H. Wilson; Thomas, James D.; Asosingh, Kewal; Comhair, Suzy A.; DiFilippo, Frank P.; Neumann, Donald R.; Davis, Laura; Graham, Brian B.; Tuder, Rubin M.; Dostanic, Iva

2013-01-01

161

Abnormal Stress?Related Measures of Arterial Stiffness in Middle?Aged and Elderly Men and Women With Impaired Fasting Glucose at Risk for a First Episode of Symptomatic Heart Failure  

PubMed Central

Background Abnormal resting arterial stiffness is present in middle?aged and elderly persons with abnormalities of fasting glucose (diabetes or impaired fasting glucose) and is associated with exercise intolerance. We sought to determine whether these same persons exhibited stress?related abnormalities of arterial stiffness. Methods and Results We analyzed dobutamine magnetic resonance stress imaging results from 373 consecutively recruited persons aged 55 to 85 years with normal fasting glucose, impaired fasting glucose, or diabetes who were at risk for but without symptomatic heart failure. Personnel blinded to participant identifiers measured arterial stiffness (brachial pulse pressure/left ventricular stroke volume indexed to body surface area, the aortic elastance index [brachial end?systolic pressure/left ventricular stroke volume indexed to body surface area], and thoracic aortic distensibility) at 80% of the maximum predicted heart rate response for age. Participants averaged 69±8 years of age; 79% were white, 92% were hypertensive, and 66% were women. After accounting for hypertension, sex, coronary artery disease, smoking, medications, hypercholesterolemia, and visceral fat, we observed an effect of glycemic status for stress measures of arterial stiffness in those with diabetes and impaired fasting glucose relative to those with normal fasting glucose (P=0.002, P=0.02, and P=0.003, respectively). Conclusion Middle? and older?aged individuals with diabetes or impaired fasting glucose have higher stress measures of arterial stiffness than those with normal fasting glucose. These data emphasize the need for future studies with larger sample sizes to determine whether stress?related elevations in arterial stiffness are related to exercise intolerance and future episodes of heart failure experienced by those with abnormalities of fasting glucose. Clinical Trial Registration URL: http://clinicaltrials.gov/. Unique identifier: NCT00542503. PMID:25589534

Vasu, Sujethra; Morgan, Timothy M.; Kitzman, Dalane W.; Bertoni, Alain; Stacey, Richard B.; Hamilton, Craig; Chiles, Caroline; Thohan, Vinay; Hundley, W. Gregory

2015-01-01

162

Lactose intolerance and other disaccharidase deficiency.  

PubMed

Intolerance to foods which contain lactose can cause a range of intestinal and systemic symptoms. These symptoms are caused by Lactase deficiency which is encoded by a single gene (LCT) of ? 50 kb located on chromosome 2q21. In some food items, lactose has been missed because of "hidden" lactose due to inadequately labeled, confusing diagnosis of lactose intolerance based on dietary restriction of dairy foods. Two polymorphisms, C/T13910 and G/A22018, linked to hypolactasia, correlate with breath hydrogen and symptoms after lactose. The key in the management of lactose intolerance is the dietary removal of lactose. Patients diagnosed as lactose intolerant must be advised of "risk" foods, inadequately labeled, including processed meats, bread, cake mixes, soft drinks, and lagers. This review highlights the types, symptoms and management of lactose intolerance and also highlights differences from milk allergy which closely mimics the symptoms of lactose intolerance. PMID:24596060

Tomar, Balvir S

2014-09-01

163

Chromium, glucose tolerance, and diabetes  

Microsoft Academic Search

Summary  Chromium functions in maintaining normal glucose tolerance primarily by regulating insulin action. In the presence of optimal\\u000a amounts of biologically active chromium, much lower amounts of insulin are required. Glucose intolerance, related to insufficient\\u000a dietary chromium, appears to be widespread. Improved chromium nutrition leads to improved sugar metabolism in hypoglycemics,\\u000a hyperglycemics, and diabetics.

Richard A. Anderson

1992-01-01

164

Aspirin Intolerance in Patients with Chronic Sinusitis  

Microsoft Academic Search

Aspirin intolerance in patients with chronic sinusitis is often a cause of early recurrence of symptoms after surgical treatment. This study assesses 84 patients who were tested for acetylsalicylic acid intolerance after presenting with symptoms like chronic rhinosinusitis, sometimes bronchial asthma, coexisting allergies or a history of aspirin sensitivity. Nasal polyposis was found in a majority of cases, often recurrent

Jan Gosepath; Frank Hoffmann; Dirk Schäfer; Ronald G. Amedee; Wolf J. Mann

1999-01-01

165

Worry, Intolerance of Uncertainty, and Statistics Anxiety  

ERIC Educational Resources Information Center

Statistics anxiety is a problem for most graduate students. This study investigates the relationship between intolerance of uncertainty, worry, and statistics anxiety. Intolerance of uncertainty was significantly related to worry, and worry was significantly related to three types of statistics anxiety. Six types of statistics anxiety were…

Williams, Amanda S.

2013-01-01

166

Lactose Intolerance: Information for Health Care Providers  

E-print Network

Lactose Intolerance: Information for Health Care are at or above their adequate intake of calcium.1 And adolescents who may be lactose intolerant are even less of their adult bone mass is established. As a health care provider, you can help your patients get the calcium

Rau, Don C.

167

Management of portal hypertension  

PubMed Central

Treatment of portal hypertension is evolving based on randomised controlled trials. In acute variceal bleeding, prophylactic antibiotics are mandatory, reducing mortality as well as preventing infections. Terlipressin or somatostatin combined with endoscopic ligation or sclerotherapy is the best strategy for control of bleeding but there is no added effect of vasoactive drugs on mortality. Non-selective ß-blockers are the first choice therapy for both secondary and primary prevention; if contraindications or intolerance to ß-blockers are present then band ligation should be used. Novel therapies target the increased intrahepatic resistance caused by microcirculatory intrahepatic deficiency of nitric oxide and contraction of activated intrahepatic stellate cells. PMID:15537846

Samonakis, D; Triantos, C; Thalheimer, U; Patch, D; Burroughs, A

2004-01-01

168

Space Flight Orthostatic Intolerance Protection  

NASA Technical Reports Server (NTRS)

This paper summarizes investigations conducted on different orthostatic intolerance protection garments. This paper emphasizes on the engineering and operational aspects of the project. The current Shuttle pneumatic Anti-G Suit or AGS at 25 mmHg (0.5 psi) and customized medical mechanical compressive garments (20-30 mmHg) were tested on human subjects. The test process is presented. The preliminary results conclude that mechanical compressive garments can ameliorate orthostatic hypotension in hypovolemic subjects. A mechanical compressive garment is light, small and works without external pressure gas source; however the current garment design does not provide an adjustment to compensate for the loss of mass and size in the lower torso during long term space missions. It is also difficult to don. Compression garments that do not include an abdominal component are less effective countermeasures than garments which do. An early investigation conducted by the Human Adaptation and Countermeasures Division at Johnson Space Center (JSC) has shown there is no significant difference between the protection function of the AGS (at 77 mmHg or 1.5 psi) and the Russian anti-g suit, Kentavr (at 25 mmHg or 0.5 psi). Although both garments successfully countered hypovolemia-induced orthostatic intolerance, the Kentavr provided protection by using lower levels of compression pressure. This more recent study with a lower AGS pressure shows that pressures at 20-30 mmHg is acceptable but protection function is not as effective as higher pressure. In addition, a questionnaire survey with flight crewmembers who used both AGS and Kentavr during different missions was also performed.

Luty, Wei

2009-01-01

169

Correlating the amount of urea, creatinine, and glucose in urine from patients with diabetes mellitus and hypertension with the risk of developing renal lesions by means of Raman spectroscopy and principal component analysis  

NASA Astrophysics Data System (ADS)

Patients with diabetes mellitus and hypertension (HT) diseases are predisposed to kidney diseases. The objective of this study was to identify potential biomarkers in the urine of diabetic and hypertensive patients through Raman spectroscopy in order to predict the evolution to complications and kidney failure. Urine samples were collected from control subjects (CTR) and patients with diabetes and HT with no complications (lower risk, LR), high degree of complications (higher risk, HR), and doing blood dialysis (DI). Urine samples were stored frozen (-20°C) before spectral analysis. Raman spectra were obtained using a dispersive spectrometer (830-nm, 300-mW power, and 20-s accumulation). Spectra were then submitted to principal component analysis (PCA) followed by discriminant analysis. The first PCA loading vectors revealed spectral features of urea, creatinine, and glucose. It has been found that the amounts of urea and creatinine decreased as disease evoluted from CTR to LR/HR and DI (PC1, p<0.05), and the amount of glucose increased in the urine of LR/HR compared to CTR (PC3, p<0.05). The discriminating model showed better overall classification rate of 70%. These results could lead to diagnostic information of possible complications and a better disease prognosis.

Bispo, Jeyse Aliana Martins; de Sousa Vieira, Elzo Everton; Silveira, Landulfo; Fernandes, Adriana Barrinha

2013-08-01

170

Metabolic syndrome in hypertensive patients: An unholy alliance  

PubMed Central

For many years, it has been recognized that hypertension tends to cluster with various anthropometric and metabolic abnormalities including abdominal obesity, elevated triglycerides, reduced high-density lipoprotein cholesterol, glucose intolerance, insulin resistance and hyperuricemia. This constellation of various conditions has been transformed from a pathophysiological concept to a clinical entity, which has been defined metabolic syndrome (MetS). The consequences of the MetS have been difficult to assess without commonly accepted criteria to diagnose it. For this reason, on 2009 the International Diabetes Federation, the American Heart Association and other scientific organizations proposed a unified MetS definition. The incidence of the MetS has been increasing worldwide in parallel with an increase in overweight and obesity. The epidemic proportion reached by the MetS represents a major public health challenge, because several lines of evidence showed that the MetS, even without type 2 diabetes, confers an increased risk of cardiovascular morbidity and mortality in different populations including also hypertensive patients. It is likely that the enhanced cardiovascular risk associated with MetS in patients with high blood pressure may be largely mediated through an increased prevalence of preclinical cardiovascular and renal changes, such as left ventricular hypertrophy, early carotid atherosclerosis, impaired aortic elasticity, hypertensive retinopathy and microalbuminuria. Indeed, many reports support this notion, showing that hypertensive patients with MetS exhibit, more often than those without it, these early signs of end organ damage, most of which are recognized as significant independent predictors of adverse cardiovascular outcomes. PMID:25276291

Mulè, Giuseppe; Calcaterra, Ilenia; Nardi, Emilio; Cerasola, Giovanni; Cottone, Santina

2014-01-01

171

Short-term low-dose growth hormone administration in subjects with impaired glucose tolerance and the metabolic syndrome: effects on beta-cell function and post-load glucose tolerance  

Microsoft Academic Search

Objective: Modest elevations in circulating IGF-I levels have been suggested to protect against the development of glucose intolerance in insulin-resistant subjects. To further understand the inter- actions of GH and IGF-I on b-cell function and post-load glucose tolerance in glucose-intolerant sub- jects predisposed to diabetes, we performed a pilot study in 12 subjects with impaired glucose tolerance and the metabolic

Kevin Yuen; Nicholas Wareham; Jan Frystyk; Susie Hennings; Jo Mitchell; Linda Fryklund; David Dunger

2004-01-01

172

Toward universal criteria for gestational diabetes: The 75-gram glucose tolerance test in pregnancy  

Microsoft Academic Search

OBJECTIVES: The purpose of this study was to determine the distribution of values for the 75 gm glucose tolerance test in pregnancy and to define glucose intolerance by the relationship between maternal glucose values and neonatal macrosomia.STUDY DESIGN: A total 3505 unselected pregnant women were given a 75 gm, 2-hour glucose tolerance test. Diet or insulin therapy was offered only

David A. Sacks; Jeffrey S. Greenspoon; Salim Abu-Fadil; Harold M. Henry; Girma Wolde-Tsadik; Janis F. F. Yao

1995-01-01

173

Milk for Kids with Lactose Intolerance  

MedlinePLUS

... of Young Children, USDA, Food and Nutrition Service Lactose Intolerance is… A food sensitivity, not a milk allergy or sickness! It happens when the body does not make enough lactase. Lactase is a body enzyme that handles lactose, ...

174

Lactose intolerance: from diagnosis to correct management.  

PubMed

This review discusses one of the most relevant problems in gastrointestinal clinical practice: lactose intolerance. The role of lactase-persistence alleles the diagnosis of lactose malabsorption the development of lactose intolerance symptoms and its management. Most people are born with the ability to digest lactose, the major carbohydrate in milk and the main source of nutrition until weaning. Approximately, 75% of the world's population loses this ability at some point, while others can digest lactose into adulthood. Symptoms of lactose intolerance include abdominal pain, bloating, flatulence and diarrhea with a considerable intraindividual and interindividual variability in the severity. Diagnosis is most commonly performed by the non invasive lactose hydrogen breath test. Management of lactose intolerance consists of two possible clinical choice not mutually exclusive: alimentary restriction and drug therapy. PMID:24443063

Di Rienzo, T; D'Angelo, G; D'Aversa, F; Campanale, M C; Cesario, V; Montalto, M; Gasbarrini, A; Ojetti, V

2013-01-01

175

Mechanisms of post-flight orthostatic intolerance  

NASA Technical Reports Server (NTRS)

Post-flight orthostatic intolerance is a dramatic physiological consequence of human adaptation to microgravity made inappropriate by a sudden return to 1-G. The immediate mechanism is almost always a failure to maintain adequate tissue perfusion, specifically perfusion of the central nervous system, but vestibular dysfunction may occasionally be the primary cause. Orthostatic intolerance is present in a wide range of clinical disorders of the nervous and cardiovascular systems. The intolerance that is produced by spaceflight and 1-G analogs (bed rest, head-down tilt at a moderate angle, water immersion) is different from its clinical counterparts by being only transiently present in subjects who otherwise have normal cardiovascular and regulatory systems. However, the same set of basic pathophysiological elements should be considered in the analysis of any form of orthostatic intolerance.

Blomqvist, C. G.; Buckey, J. C.; Gaffney, F. A.; Lane, L. D.; Levine, B. D.; Watenpaugh, D. E.

1994-01-01

176

Diabetic population mortality and cardiovascular risk attributable to hypertension: a decade follow-up from the Tehran Lipid and Glucose Study.  

PubMed

To determine the extent to which burden of cardiovascular disease (CVD) outcomes among diabetic population is attributable to hypertension. Nine-year follow-up data were secured for 7068 participants aged ? 20 years old, free from CVD at baseline. Cox proportional hazards regression was implemented to estimate hazard ratios (HRs) of hypertension. Population-attributable hazard fraction (PAHF) was used to assess proportion of diabetic population hazard of CVD events and mortality attributable to hypertension. In the whole population, irrespective of diabetes or hypertension status, incidence rate (95% CI) of CVD, coronary heart disease (CHD), as well as CVD and all-cause mortality per 1000 person-year were 8.3 (7.6-9.0), 7.1 (6.5-7.8), 1.8 (1.5-2.1) and 3.9 (3.5-4.5), respectively. Among diabetes participants, hypertension was a risk factor for CHD (HR = 1.63, 95% CI 1.15-2.03), CVD (HR = 1.74, 95% CI 1.50-2.41), CVD mortality (HR = 1.65, 95% CI 0.87-3.12) and all-cause mortality (HR = 1.53, 95% CI 0.97-2.42). HRs, however, were not statistically significant for all-cause or CVD mortality. PAHFs (%) of hypertension was 27.5 (95% CI 8.3-42.6) for CHD, 29.6 (95% CI 10.6-44.4) for CVD, 27.9 (95% CI - 17.2 to 55.7) for CVD mortality and 22.6 (95% CI - 5.9 to 43.4) for all-cause mortality. Our study shows that there is an excess risk of CVD in hypertensive patients with diabetes related to inadequate control of blood pressure. PMID:23458066

Bozorgmanesh, Mohammadreza; Hadaegh, Farzad; Mohebi, Reza; Ghanbarian, Arash; Eskandari, Fatemeh; Azizi, Fereidoun

2013-10-01

177

Decreased physical fitness in borderline glucose tolerance men  

Microsoft Academic Search

To investigate the primary changes in glucose intolerance, physical characteristics and daily-life activity (pattern) were\\u000a compared in the normal glucose tolerance (NGT, n=7) and the borderline glucose tolerance (BGT, n=9) subjects based on the\\u000a criteria adopted by the Committee on the Diagnosis of Diabetes mellitus of Japan Diabetes Society. The basal glucose and insulin\\u000a concentrations in the BGT group (90.7±4.1mg\\/dl,

Yasuki Higaki; Naoko Shono; Masahiro Nishizumi

1998-01-01

178

Improvements in glucose tolerance in obese males with abnormal glucose tolerance following 10 days of aerobic exercise  

Microsoft Academic Search

Background. Aerobic exercise training has been shown to produce beneficial changes in glucose tolerance and insulin sensitivity in obese individuals if performed at high enough intensities and\\/or durations. We examined the effects of a moderate intensity, short-term exercise training protocol on glucose tolerance in obese males with glucose intolerance.Methods. Fourteen abdominally obese, sedentary males with normal glucose tolerance (NGT; n

Julia C Denton; Rebecca Schultz; Athanasios Z Jamurtas; Theodore J Angelopoulos

2004-01-01

179

Nervous glucose sensing regulates postnatal ? cell proliferation and glucose homeostasis  

PubMed Central

How glucose sensing by the nervous system impacts the regulation of ? cell mass and function during postnatal development and throughout adulthood is incompletely understood. Here, we studied mice with inactivation of glucose transporter 2 (Glut2) in the nervous system (NG2KO mice). These mice displayed normal energy homeostasis but developed late-onset glucose intolerance due to reduced insulin secretion, which was precipitated by high-fat diet feeding. The ? cell mass of adult NG2KO mice was reduced compared with that of WT mice due to lower ? cell proliferation rates in NG2KO mice during the early postnatal period. The difference in proliferation between NG2KO and control islets was abolished by ganglionic blockade or by weaning the mice on a carbohydrate-free diet. In adult NG2KO mice, first-phase insulin secretion was lost, and these glucose-intolerant mice developed impaired glucagon secretion when fed a high-fat diet. Electrophysiological recordings showed reduced parasympathetic nerve activity in the basal state and no stimulation by glucose. Furthermore, sympathetic activity was also insensitive to glucose. Collectively, our data show that GLUT2-dependent control of parasympathetic activity defines a nervous system/endocrine pancreas axis that is critical for ? cell mass establishment in the postnatal period and for long-term maintenance of ? cell function. PMID:24334455

Tarussio, David; Metref, Salima; Seyer, Pascal; Mounien, Lourdes; Vallois, David; Magnan, Christophe; Foretz, Marc; Thorens, Bernard

2013-01-01

180

Nervous glucose sensing regulates postnatal ? cell proliferation and glucose homeostasis.  

PubMed

How glucose sensing by the nervous system impacts the regulation of ? cell mass and function during postnatal development and throughout adulthood is incompletely understood. Here, we studied mice with inactivation of glucose transporter 2 (Glut2) in the nervous system (NG2KO mice). These mice displayed normal energy homeostasis but developed late-onset glucose intolerance due to reduced insulin secretion, which was precipitated by high-fat diet feeding. The ? cell mass of adult NG2KO mice was reduced compared with that of WT mice due to lower ? cell proliferation rates in NG2KO mice during the early postnatal period. The difference in proliferation between NG2KO and control islets was abolished by ganglionic blockade or by weaning the mice on a carbohydrate-free diet. In adult NG2KO mice, first-phase insulin secretion was lost, and these glucose-intolerant mice developed impaired glucagon secretion when fed a high-fat diet. Electrophysiological recordings showed reduced parasympathetic nerve activity in the basal state and no stimulation by glucose. Furthermore, sympathetic activity was also insensitive to glucose. Collectively, our data show that GLUT2-dependent control of parasympathetic activity defines a nervous system/endocrine pancreas axis that is critical for ? cell mass establishment in the postnatal period and for long-term maintenance of ? cell function. PMID:24334455

Tarussio, David; Metref, Salima; Seyer, Pascal; Mounien, Lourdes; Vallois, David; Magnan, Christophe; Foretz, Marc; Thorens, Bernard

2014-01-01

181

Prevalence and Predictors of Risk for Type 2 Diabetes Mellitus and Impaired Glucose Tolerance in Polycystic Ovary Syndrome: A Prospective, Controlled Study in 254 Affected Women  

Microsoft Academic Search

Women with polycystic ovary syndrome (PCOS) are insulin resis- tant, have insulin secretory defects, and are at high risk for glucose intolerance. We performed this study to determine the prevalence of glucose intolerance and parameters associated with risk for this in PCOS women. Two-hundred and fifty-four PCOS women, aged 14 - 44 yr, were prospectively evaluated at 2 centers, 1

RICHARD S. LEGRO; ALLEN R. KUNSELMAN; WILLIAM C. DODSON; ANDREA DUNAIF

182

Acarbose for the prevention of Type 2 diabetes, hypertension and cardiovascular disease in subjects with impaired glucose tolerance: facts and interpretations concerning the critical analysis of the STOP-NIDDM Trial data.  

PubMed

The STOP-NIDDM Trial has shown that acarbose treatment in subjects with impaired glucose tolerance is associated with a significant risk reduction in the development of diabetes, hypertension and cardiovascular complications. Kaiser and Sawicki have accused the investigators of the STOP-NIDDM Trial of major biases in the conduct of the study, of manipulating the data and of conflict of interest. The aim of this paper is to present data and explanations refuting these allegations. In the STOP-NIDDM Trial, 61 subjects were excluded from the efficacy analysis before unblinding for legitimate reasons: failure to satisfy major entry criteria (n=17) and lack of post-randomisation data (n=44). Blinding and randomisation were carried out by an independent biostatistician. Titration of placebo/acarbose is well described in the protocol and in the study design paper. Of the study population, 9.3% had a fasting plasma glucose of > or =7.0 mmol/l at screening and could have been diabetic according to the new diagnostic criteria. However, even if these subjects are excluded, patients having acarbose treatment still saw a significant risk reduction in the development of diabetes (p=0.0027). The changes in weight are consistent in different publications and are related to different times of follow-up and assessment. Weight change does have an effect on the development of diabetes, but acarbose treatment is still effective even after adjusting for this (p=0.0063). The cardiovascular endpoints were a clearly designated assessment in the original protocol, and only those defined in the protocol and ascertained by the independent Cardiovascular Event Adjudication Committee were used in the analysis. Hypertension was defined according to the most recent diagnostic criteria. The STOP-NIDDM Trial results are scientifically sound and credible. The investigators stand strongly behind these results demonstrating that acarbose treatment is associated with a delay in the development of diabetes, hypertension and cardiovascular complications in a high-risk population with IGT. PMID:15164169

Chiasson, J-L; Josse, R G; Gomis, R; Hanefeld, M; Karasik, A; Laakso, M

2004-06-01

183

Growth Hormone and Glucose Homeostasis  

Microsoft Academic Search

Patients with active acromegaly are insulin-resistant and glucose-intolerant, whereas children with growth hormone (GH) deficiency (GHD) are insulin-sensitive and may develop fasting hypoglycaemia. Surprisingly, however, hypopituitary adults with unsubstituted GHD tend to be insulin-resistant, which may worsen during GH substitution. During fasting, which may be considered the natural domain for the metabolic effects of GH, the induction of insulin resistance

Jens O. L. Jørgensen; Morten Krag; Niels Jessen; Helene Nørrelund; Esben T. Vestergaard; Niels Møller; Jens S. Christiansen

2004-01-01

184

Senegal: growing intolerance towards gay men.  

PubMed

The arrest and conviction of nine gay men in Senegal in January 2009 is part of a disturbing pattern. A largely Muslim country, Senegal has become increasing intolerant of homosexuality in recent years, despite having a reputation for liberalism and openness. PMID:19610208

2009-05-01

185

ARTICLE doi:10.1038/nature13793 Artificial sweeteners induce glucose  

E-print Network

of NAS on glucose homeostasis, we added commercial formulations of saccharin, sucralose or aspartameARTICLE doi:10.1038/nature13793 Artificial sweeteners induce glucose intolerance by altering we demonstrate that consumption of commonly used NAS formulations drives the development of glucose

Gleeson, Joseph G.

186

The Importance of a Postpartum 75 g Oral Glucose Tolerance Test in Women With Gestational Diabetes  

Microsoft Academic Search

Objective: To compare the ability of the fasting plasma glucose (FPG) level with the ability of the 2-hour oral glucose tolerance test (OGTT) to identify women with any form of glucose intolerance within the first six postpartum months. Methods: In a retrospective, observational analysis, the predictive ability of the FPG level was compared with that of the 2-hour OGTT in

Shauna L. Reinblatt; Lucie Morin; Sara J. Meltzer; Montreal QC

2006-01-01

187

Severity of HCV-Induced Liver Damage Alters Glucose Homeostasis in Noncirrhotic Patients with Chronic HCV Infection  

Microsoft Academic Search

Background\\/Aims: To investigate the link between hepatitis C infection and glucose intolerance, we measured insulin sensitivity, glucose effectiveness and ?-cell secretion in noncirrhotic HCV-infected patients with normal glucose tolerance according to WHO criteria as assessed by oral glucose tolerance tests. Methods: Glucose, insulin and C-peptide data from frequently sampled intravenous glucose tolerance tests were analyzed using the minimal modeling technique

T. Konrad; S. Zeuzem; G. Toffolo; P. Vicini; G. Teuber; D. Briem; J. Lormann; T. Lenz; G. Herrmann; A. Berger; C. Cobelli; K.-H. Usadel

2000-01-01

188

Exercise Pathophysiology in Patients With Primary Pulmonary Hypertension  

Microsoft Academic Search

Background—Patients with primary pulmonary hypertension (PPH) have a pulmonary vasculopathy that leads to exercise intolerance due to dyspnea and fatigue. To better understand the basis of the exercise limitation in patients with PPH, cardiopulmonary exercise testing (CPET) with gas exchange measurements, New York Heart Association (NYHA) symptom class, and resting pulmonary hemodynamics were studied. Methods and Results—We retrospectively evaluated 53

Xing-Guo Sun; James E. Hansen; Ronald J. Oudiz; Karlman Wasserman

2008-01-01

189

Nutritional regulation of hepatic glucose metabolism in fish  

Microsoft Academic Search

Glucose plays a key role as energy source in the majority of mammals, but its importance in fish appears limited. Until now,\\u000a the physiological basis for such apparent glucose intolerance in fish has not been fully understood. A distinct regulation\\u000a of hepatic glucose utilization (glycolysis) and production (gluconeogenesis) may be advanced to explain the relative inability\\u000a of fish to efficiently

P. Enes; S. Panserat; S. Kaushik; A. Oliva-Teles

2009-01-01

190

Portopulmonary hypertension.  

PubMed

The development of pulmonary arterial hypertension in the setting of portal hypertension is known as portopulmonary hypertension. Portal hypertension is thought to predispose patients to disturbances in the homeostatic regulation of numerous neurohumoral and vasoactive mediators that induce the development of pulmonary arterial hypertension. Portopulmonary hypertension is pathologically indistinguishable from idiopathic pulmonary arterial hypertension and is characterized by the development of vasoconstriction, vascular remodeling, and thrombosis within the pulmonary vasculature. Although described in patients with both cirrhotic and noncirrhotic portal hypertension, portopulmonary hypertension is most prevalent among patients with end-stage liver disease, and its severity seems to be independent of the etiology or severity of liver disease. All liver transplant candidates must be screened for the presence of portopulmonary hypertension because of the high perioperative mortality risk of liver transplantation associated with this condition. Primary screening for portopulmonary hypertension consists of Doppler-estimated pulmonary artery systolic pressure measurement during echocardiography. However, the diagnosis of portopulmonary hypertension is based on unique hemodynamic criteria as determined by right heart catheterization. Untreated portopulmonary hypertension portends a poor prognosis, and the efficacy of current treatment modalities is limited. At present, the primary goals of therapy are to provide symptomatic relief, prolong survival, and improve pulmonary hemodynamics to facilitate safe and successful liver transplantation. PMID:21325952

Mukhtar, Nizar A; Fix, Oren K

2011-09-01

191

Lactose intolerance: diagnosis, genetic, and clinical factors.  

PubMed

Most people are born with the ability to digest lactose, the major carbohydrate in milk and the main source of nutrition until weaning. Approximately 75% of the world's population loses this ability at some point, while others can digest lactose into adulthood. This review discusses the lactase-persistence alleles that have arisen in different populations around the world, diagnosis of lactose intolerance, and its symptomatology and management. PMID:22826639

Mattar, Rejane; de Campos Mazo, Daniel Ferraz; Carrilho, Flair José

2012-01-01

192

Fanconi syndrome with lysinuric protein intolerance  

PubMed Central

We present the case of a 9-year-old child with lysinuric protein intolerance and Fanconi syndrome. She was referred to our hospital with a persistent metabolic acidosis and polyuria. Renal investigations revealed all laboratory signs of Fanconi syndrome, with glucosuria, generalized aminoaciduria, phosphaturia and severe hypercalciuria. The diagnosis of Fanconi syndrome was confirmed by a renal biopsy that showed extensive lesions of proximal tubular epithelial cells with vacuolation of these cells and a sloughing of the brush border.

Riccio, Eleonora; Pisani, Antonio

2014-01-01

193

Management of the Patient with Statin Intolerance  

Microsoft Academic Search

Current guidelines recommend statins as first-line therapy for reducing low-density lipoprotein cholesterol (LDL-C) and preventing\\u000a cardiovascular events. Patients taking statins frequently experience adverse effects during therapy. The first step is to\\u000a determine whether the adverse effects are indeed related to statin therapy by statin dechallenge and rechallenge. Strategies\\u000a for managing statin intolerance include changing statins, intermittent dosing, intensification of lifestyle

Byron F. Vandenberg; Jennifer Robinson

2010-01-01

194

Renovascular hypertension  

MedlinePLUS

Renal hypertension; Hypertension - renovascular; Renal artery occlusion; Stenosis - renal artery; Renal artery stenosis ... Renal artery stenosis is a narrowing or blockage of the arteries that supply blood to the kidneys. The most ...

195

Malignant hypertension  

MedlinePLUS

... for malignant hypertension if you have had: Kidney failure Renal hypertension caused by renal artery stenosis ... An eye examination will reveal changes that indicate high blood ... failure, as well as other complications, may develop. Tests ...

196

Statin intolerance: now a solved problem.  

PubMed

Statins are the most effective and widely used drugs for treating dyslipidemia, a major risk factor for coronary heart disease. These are one of the safest hypolipidemic drugs but many patients are bound to discontinue statins due to their side effects. Hepatotoxicity, myotoxicity and peripheral neuropathy are important out of them. Discontinuation of statins leads to dylipidemia and its grave consequences. Hence, there should be enough strategies for statin intolerant patients, so that they can be saved from these consequences. These side effects can be avoided by the awareness of certain factors viz. potential drug interactions and dose adjustment according to patho-physiology of the patient. Baseline investigations for liver function and muscle toxicity should be done before initiating statin therapy. Here, we are discussing various options for statin intolerant hyperlipidemic patients such as lower and intermittent dosing of statins, alternate hypolipidemic drugs, red yeast rice, supplementation with coenzyme Q10 and vitamin D. A number of hypolipidemic drugs are in trial phases and hold promise for statin intolerant patients. PMID:22120862

Sikka, P; Kapoor, S; Bindra, V K; Sharma, M; Vishwakarma, P; Saxena, K K

2011-01-01

197

Idiopathic orthostatic intolerance and postural tachycardia syndromes  

NASA Technical Reports Server (NTRS)

Upright posture imposes a substantial gravitational stress on the body, for which we are able to compensate, in large part because of the autonomic nervous system. Alteration in autonomic function, therefore, may lead to orthostatic intolerance. On one extreme, patients with autonomic failure caused by degenerative loss of autonomic function are severely disabled by orthostatic hypotension and may faint whenever they stand up. Fortunately, such patients are relatively rare. On the other hand, disabling orthostatic intolerance can develop in otherwise normal young people. These patients can be severely impaired by symptoms of fatigue, tachycardia, and shortness of breath when they stand up. The actual incidence of this disorder is unknown, but these patients make up the largest group of patients referred to centers that specialize in autonomic disorders. We will review recent advances made in the understanding of this condition, potential pathophysiological mechanisms that contribute to orthostatic intolerance, therapeutic alternatives currently available for the management of these patients, and areas in which more research is needed.

Jacob, G.; Biaggioni, I.; Robertson, D. (Principal Investigator)

1999-01-01

198

Sucrose feeding in mouse pregnancy leads to hypertension, and sex-linked obesity and insulin resistance in female offspring  

PubMed Central

Eating an unbalanced diet during pregnancy may induce long-term health consequences in offspring, in particular obesity, insulin resistance, and hypertension. We tested the hypothesis that a maternal diet rich in simple sugars predispose mouse offspring to obesity, glucose intolerance, and cardiovascular diseases in adulthood. Female C57BL/6J mice were fed either a standard chow or a sucrose-rich diet (26% of total energy) 6 weeks prior to mating, throughout pregnancy and lactation. Offspring of control dams (OC) and high sucrose fed dams (OSF) were weaned onto standard control chow, and metabolic and cardiovascular parameters determined at 3 months of age. Both male and female OSF were hyperphagic by 4 weeks of age and females were heavier than OC at 6 weeks. At 3 months, female OSF showed a significant increase in inguinal fat pad mass, whereas skeletal muscle mass (tibialis anterior) and locomotor activity were decreased relative to OC. A 10-fold increase in fasting serum insulin in female OSF vs. OC at 3 months (Insulin [pmol/L] mean ± SEM, OSF, 200.3 ± 16.1, vs. OC, 20.3 ± 1.8, n = 6 P < 0.001), was associated with impaired glucose tolerance (AUC [mmol/L min] mean ± SEM, OSF 1437.4 ± 124.2 vs. OC, 1076.8 ± 83.9, n = 6, P < 0.05). Both male and female OSF were hypertensive as assessed by radiotelemetry (night-time systolic arterial pressure (SAP) [mmHg] mean ± SEM, male OSF, 128 ± 1 vs. OC, 109 ± 1, n = 6, P < 0.01; female OSF, 130 ± 1 vs. OC, 118 ± 1, n = 6, P < 0.05). Analysis of heart rate variability (HRV) demonstrated an increased low:high frequency ratio in male and female OSF (P < 0.05), indicative of heightened sympathetic efferent tone. Renal tissue noradrenaline (NA) content was markedly raised in the OSF vs. OC (NA [pg/ml/mg tissue] mean ± SEM, male OSF, 2.28 ± 0.19 vs. OC 0.84 ± 0.09, n = 6, P < 0.01). Exposure to a maternal diet rich in sucrose led to obesity and glucose intolerance in female mice offspring, and hypertension in both sexes. PMID:23423541

Samuelsson, Anne-Maj; Matthews, Phillippa A.; Jansen, Eugene; Taylor, Paul D.; Poston, Lucilla

2013-01-01

199

Chronic Hypertension in Pregnancy  

MedlinePLUS

... Hypertension? There are 2 types of chronic hypertension: essential hypertension and secondary hypertension. We do not know the cause of essential hypertension, but because hypertension commonly runs in families, we ...

200

Hypovolemia in syncope and orthostatic intolerance role of the renin-angiotensin system  

NASA Technical Reports Server (NTRS)

PURPOSE: Orthostatic intolerance is the cause of significant disability in otherwise normal patients. Orthostatic tachycardia is usually the dominant hemodynamic abnormality, but symptoms may include dizziness, visual changes, discomfort in the head or neck, poor concentration, fatigue, palpitations, tremulousness, anxiety and, in some cases, syncope. It is the most common disorder of blood pressure regulation after essential hypertension. There is a predilection for younger rather than older adults and for women more than men. Its cause is unknown; partial sympathetic denervation or hypovolemia has been proposed. METHODS AND MATERIALS: We tested the hypothesis that reduced plasma renin activity, perhaps from defects in sympathetic innervation of the kidney, could underlie a hypovolemia, giving rise to these clinical symptoms. Sixteen patients (14 female, 2 male) ranging in age from 16 to 44 years were studied. Patients were enrolled in the study if they had orthostatic intolerance, together with a raised upright plasma norepinephrine (> or = 600 pg/mL). Patients underwent a battery of autonomic tests and biochemical determinations. RESULTS: There was a strong positive correlation between the blood volume and plasma renin activity (r = 0.84, P = 0.001). The tachycardic response to upright posture correlated with the severity of the hypovolemia. There was also a correlation between the plasma renin activity measured in these patients and their concomitant plasma aldosterone level. CONCLUSIONS: Hypovolemia occurs commonly in orthostatic intolerance. It is accompanied by an inappropriately low level of plasma renin activity. The degree of abnormality of blood volume correlates closely with the degree of abnormality in plasma renin activity. Taken together, these observations suggest that reduced plasma renin activity may be an important pathophysiologic component of the syndrome of orthostatic intolerance.

Jacob, G.; Robertson, D.; Mosqueda-Garcia, R.; Ertl, A. C.; Robertson, R. M.; Biaggioni, I.

1997-01-01

201

Genetic variation in aldosterone synthase predicts plasma glucose levels  

E-print Network

predisposing genes for essential hypertension and insulin resistance. To maximize our chances of finding for aldosterone in glucose homeostasis. Hypertension affects 15­50% of the adult population and is one understanding of heritable factors in the etiology of hypertension is rather poor. Twin, adoption

Botstein, David

202

A current approach to statin intolerance.  

PubMed

Statins are the first-line pharmacotherapy for cholesterol reduction. Use of these drugs in large randomized clinical trials has consistently shown significant reductions in major vascular events, including death, myocardial infarction, stroke, and coronary revascularization. The updated guidelines for the treatment of high blood cholesterol from the American College of Cardiology/American Heart Association (ACC/AHA), will lead to an increase in the number of patients taking statins. Hence, the number of cases of statin intolerance may subsequently increase, emphasizing the need to understand and treat this important problem. PMID:24727470

Tompkins, R; Schwartzbard, A; Gianos, E; Fisher, E; Weintraub, H

2014-07-01

203

Antihypertensive drugs and glucose metabolism  

PubMed Central

Hypertension plays a major role in the development and progression of micro- and macrovascular disease. Moreover, increased blood pressure often coexists with additional cardiovascular risk factors such as insulin resistance. As a result the need for a comprehensive management of hypertensive patients is critical. However, the various antihypertensive drug categories have different effects on glucose metabolism. Indeed, angiotensin receptor blockers as well as angiotensin converting enzyme inhibitors have been associated with beneficial effects on glucose homeostasis. Calcium channel blockers (CCBs) have an overall neutral effect on glucose metabolism. However, some members of the CCBs class such as azelnidipine and manidipine have been shown to have advantageous effects on glucose homeostasis. On the other hand, diuretics and ?-blockers have an overall disadvantageous effect on glucose metabolism. Of note, carvedilol as well as nebivolol seem to differentiate themselves from the rest of the ?-blockers class, being more attractive options regarding their effect on glucose homeostasis. The adverse effects of some blood pressure lowering drugs on glucose metabolism may, to an extent, compromise their cardiovascular protective role. As a result the effects on glucose homeostasis of the various blood pressure lowering drugs should be taken into account when selecting an antihypertensive treatment, especially in patients which are at high risk for developing diabetes. PMID:25068013

Rizos, Christos V; Elisaf, Moses S

2014-01-01

204

Metabolic syndrome: treatment of hypertensive patients.  

PubMed

Metabolic syndrome (MetSyndr), a constellation of abnormalities [obesity, glucose intolerance, insulin resistance (IR), dyslipidemia (low HDL-cholesterol, high LDL-cholesterol and triglycerides (TG)], and elevated blood pressure (BP)], increases the risk of cardiovascular (CV) disease and premature death. From 10% to 30% of the adult population in industrialized countries has MetSyndr, which effectively predicts the development of type 2 diabetes mellitus (T2D) and CV disease. Because of the complex etiology of MetSyndr, a multi-targeted, integrated therapeutic approach is required to simultaneously treat high BP, obesity, lipid disorders and T2D (if present), to fully protect CV, cerebrovascular and renal systems. If lifestyle modification (weight control, diet, exercise, smoking cessation, moderation of alcohol intake) is ineffective, pharmaco-theraphy should be added to treat simultaneously the lipid- and non-lipid CV risk factors. Patients with HTN and MetSyndr should be started on angiotensin-converting enzyme (ACE) inhibitors, unless contraindicated. The ACE inhibitors and angiotensin receptor blockers (ARBs) reduce the odds of developing new onset T2D and also decrease albuminuria. The ACE inhibitors provide cardioprotective and renoprotective benefits beyond their effect on BP; they also improve IR. The ARBs are renoprotective in addition to being cardioprotective. Long-acting calcium channel blockers are also recommended in hypertensive patients with MetSyndr; these drugs also improve IR. Thiazides (at low doses) and selected ss-blockers can be given to patients with HTN and MetSyndr. Celiprolol in combination with diuretics has a favorable effect on glucose tolerance and IR in patients with HTN and MetSyndr, and spironolactone added to ACE inhibitor or ARB therapy provides additional reno- and CV protective benefits in patients with diabetic nephropathy. Carvedilol, a ss-blocker with vasodilating properties, added to ACE inhibitor or ARB therapy, is effective in preventing worsening of microalbuminuria in patients with HTN and MetSyndr; it also improves IR and glycemic control. Most patients eventually require two or more antihypertensive drugs to reach BP goal. It is recommended that therapy in patients whose BP is more than 20/10 mm Hg above target at diagnosis be initiated with a combination of antihypertensive drugs, administered either as individual drugs or as fixed-dose formulations. Treatment with fixed-dose combinations, such as irbesartan + hydrochlorothiazide provides good BP control in more than two-thirds of hypertensive patients with MetSyndr. Lipid and BP targets are reached in a high percent of patients with HTN and CV disease treated with a combination of amlodipine + atorvastatin. In conclusion, hypertensive patients with the MetSyndr be treated aggressively for each component of the syndrome to provide CV, cerebrovascular and renal protection. PMID:17667215

Israili, Zafar H; Lyoussi, Badiâa; Hernández-Hernández, Rafael; Velasco, Manuel

2007-01-01

205

Chemical Intolerance in Primary Care Settings: Prevalence, Comorbidity, and Outcomes  

PubMed Central

PURPOSE This study extends previous community-based studies on the prevalence and clinical characteristics of chemical intolerance in a sample of primary care clinic patients. We evaluated comorbid medical and psychiatric disorders, functional status, and rates of health care use. METHODS A total of 400 patients were recruited from 2 family medicine clinic waiting rooms in San Antonio, Texas. Patients completed the validated Quick Environmental Exposure and Sensitivity Inventory (QEESI) to assess chemical intolerance; the Primary Care Evaluation of Mental Disorders (PRIME-MD) screen for possible psychiatric disorders; the Dartmouth–Northern New England Primary Care Cooperative Information Project (Dartmouth COOP) charts for functional status; and the Healthcare Utilization Questionnaire. RESULTS Overall, 20.3% of the sample met criteria for chemical intolerance. The chemically intolerant group reported significantly higher rates of comorbid allergies and more often met screening criteria for possible major depressive disorder, panic disorder, generalized anxiety disorder, and alcohol abuse disorder, as well as somatization disorder. The total number of possible mental disorders was correlated with chemical intolerance scores (P <.001). Controlling for demographics, patients with chemical intolerance were significantly more likely to have poorer functional status, with trends toward increased medical service use when compared with non–chemically intolerant patients. After controlling for comorbid psychiatric conditions, the groups differed significantly only regarding limitations of social activities. CONCLUSIONS Chemical intolerance occurs in 1 of 5 primary care patients yet is rarely diagnosed by busy practitioners. Psychiatric comorbidities contribute to functional limitations and increased health care use. Chemical intolerance offers an etiologic explanation. Symptoms may resolve or improve with the avoidance of salient chemical, dietary (including caffeine and alcohol), and drug triggers. Given greater medication intolerances in chemical intolerance, primary care clinicians could use the QEESI to identify patients for appropriate triage to comprehensive nonpharmacologic care. PMID:22778124

Katerndahl, David A.; Bell, Iris R.; Palmer, Raymond F.; Miller, Claudia S.

2012-01-01

206

Lactose intolerance in systemic nickel allergy syndrome.  

PubMed

Some patients affected by nickel-contact allergy present digestive symptoms in addition to systemic cutaneous manifestations, falling under the condition known as systemic nickel allergy syndrome (SNAS). A nickel-related pro-inflammatory status has been documented at intestinal mucosal level. The aim of the present study is to evaluate the prevalence of lactose intolerance in patients affected by SNAS compared to a healthy population. Consecutive patients affected by SNAS referring to our departments were enrolled. The control population consisted of healthy subjects without gastrointestinal symptoms. All subjects enrolled underwent lactose breath test under standard conditions. One hundred and seventy-eight SNAS patients and 60 healthy controls were enrolled. Positivity of lactose breath test occurred in 74.7% of the SNAS group compared to 6.6% of the control group. Lactose intolerance is highly prevalent in our series of patients affected by SNAS. Based on our preliminary results, we can hypothesize that in SNAS patients, the nickel-induced pro-inflammatory status could temporarily impair the brush border enzymatic functions, resulting in hypolactasia. Further trials evaluating the effect of a nickel-low diet regimen on lactase activity, histological features and immunological pattern are needed. PMID:21658331

Cazzato, I A; Vadrucci, E; Cammarota, G; Minelli, M; Gasbarrini, A

2011-01-01

207

[Histamine intolerance--possible dermatologic sequences].  

PubMed

Although histamine intolerance (HIT) is not very frequently encountered, it can have serious consequences. Food intolerance is a non allergic hypersensitivity to food that does not include the immune system even though the symptoms are similar to those of IgE-mediated allergic reactions. HIT apparently develops as a result of an impaired diamine oxidase (DAO) activity due to gastrointestinal disease or through DAO inhibition, as well as through a genetic predisposition which was proven in a number of patients. The intake of histamine-rich foods as well as alcohol or drugs which cause either the release of histamine or the blocking of DAO can lead to various disorders in many organs (gastrointestinal system, skin, lungs, cardiovascular system and brain), depending on the expression of histamine receptors. Dermatologic sequels can be rashes, itch, urticaria, angioedema, dermatitis, eczema and even acne, rosacea, psoriasis, and other. Recognizing the symptoms due to HIT is especially important in treating such patients. The significance of HIT in patients with atopic dermatitis in whom the benefit of a low histamine diet has been proven is becoming increasingly understood recently. Because of the possibility of symptoms affecting numerous organs, a detailed history of symptoms following the intake of histamine-rich foods or drugs that interfere with histamine metabolism is essential for making the diagnosis of HIT. Considering that such symptoms can be the result of multiple factors, the existence of HIT is usually underestimated, but considerable expectations are being made from future studies. PMID:23814966

Lugovi?-Mihi?, Liborija; Seserko, Ana; Duvanci?, Tomislav; Situm, Mirna; Mihi?, Josip

2012-12-01

208

Mineralocorticoid hypertension  

PubMed Central

Hypertension affects about 10 – 25% of the population and is an important risk factor for cardiovascular and renal disease. The renin-angiotensin system is frequently implicated in the pathophysiology of hypertension, be it primary or secondary. The prevalence of primary aldosteronism increases with the severity of hypertension, from 2% in patients with grade 1 hypertension to 20% among resistant hypertensives. Mineralcorticoid hypertension includes a spectrum of disorders ranging from renin-producing pathologies (renin-secreting tumors, malignant hypertension, coarctation of aorta), aldosterone-producing pathologies (primary aldosteronism – Conns syndrome, familial hyperaldosteronism 1, 2, and 3), non-aldosterone mineralocorticoid producing pathologies (apparent mineralocorticoid excess syndrome, Liddle syndrome, deoxycorticosterone-secreting tumors, ectopic adrenocorticotropic hormones (ACTH) syndrome, congenitalvadrenal hyperplasia), and drugs with mineraocorticoid activity (locorice, carbenoxole therapy) to glucocorticoid receptor resistance syndromes. Clinical presentation includes hypertension with varying severity, hypokalemia, and alkalosis. Ratio of plasma aldosterone concentraion to plasma renin activity remains the best screening tool. Bilateral adrenal venous sampling is the best diagnostic test coupled with a CT scan. Treatment is either surgical (adrenelectomy) for unilateral adrenal disease versus medical therapy for idiopathic, ambiguous, or bilateral disease. Medical therapy focuses on blood pressure control and correction of hypokalemia using a combination of anti-hypertensives (calcium channel blockers, angiotensin converting enzyme inhibitors, or angiotensin receptor blockers) and potassium-raising therapies (mineralcorticoid receptor antagonist or potassium sparing diuretics). Direct aldosterone synthetase antagonists represent a promising future therapy. PMID:22145132

Gupta, Vishal

2011-01-01

209

75 FR 2551 - NIH Consensus Development Conference: Lactose Intolerance and Health; Notice  

Federal Register 2010, 2011, 2012, 2013, 2014

...products. Lactose intolerance is caused...the enzyme lactase, which is...products by lactase nonpersisters...symptoms of lactose intolerance are caused...attributable to lactose intolerance is difficult...and manage lactase...

2010-01-15

210

Lactose intolerance: a self-fulfilling prophecy leading to osteoporosis?  

PubMed

Symptoms of lactose intolerance are unlikely to occur under usual dietary conditions. Yet, self-described "lactose-intolerant" individuals often restrict dairy and calcium intake. A new study suggests that such individuals have reduced peak bone mass and increased incidence of osteopenia, and are at greater risk of osteoporosis and bone fractures. PMID:12903833

Savaiano, Dennis

2003-06-01

211

Intolerance and tolerance in the Jewish tradition and contemporary Israel  

Microsoft Academic Search

In this paper the author relates Jewish cultural resources to the structuring of intolerance and tolerance in the Jewish tradition. The role of collectivist and primordial orientations are highlighted not only in the definition of intolerance but in the construction of patterns of tolerance as well. Because of the decisive role of these orientations, the distinction between public and private

Shlomo Fischer

2003-01-01

212

Regulator of G protein signaling-4 controls fatty acid and glucose homeostasis  

E-print Network

Regulator of G protein signaling-4 controls fatty acid and glucose homeostasis Iankova Irena 1 2 degree of glucose intolerance, and decreased insulin secretion in pancreas. We show in this study ; liver steatosis ; insulin secretion Introduction White adipose tissue (WAT) homeostasis implicates

Boyer, Edmond

213

RGS4 controls fatty acid and glucose homeostasis Running title: RGS4 in lipid metabolism  

E-print Network

RGS4 controls fatty acid and glucose homeostasis Running title: RGS4 in lipid metabolism Irena degree of glucose intolerance, and decreased insulin secretion in pancreas. We show in this study) homeostasis implicates a complex regulatory network of signaling and transcriptional events resulting

Boyer, Edmond

214

Prevalence of methotrexate intolerance in rheumatoid arthritis and psoriatic arthritis  

PubMed Central

Introduction The aim of this study was to determine the prevalence of gastrointestinal and behavioural symptoms occurring before (anticipatory/associative) and after methotrexate (MTX) administration, termed MTX intolerance, in rheumatoid (RA) and psoriatic arthritis (PsA). Methods Methotrexate Intolerance Severity Score (MISS), previously validated in juvenile idiopathic arthritis patients, was used to determine MTX intolerance prevalence in 291 RA/PsA patients. The MISS consisted of four domains: abdominal pain, nausea, vomiting and behavioural symptoms, occurring upon, prior to (anticipatory) and when thinking of MTX (associative). MTX intolerance was defined as ?6 on the MISS with ?1 point on anticipatory and/or associative and/or behavioural items. Results A total of 123 patients (42.3%) experienced at least one gastrointestinal adverse effect. The prevalence of MTX intolerance was 11%. MTX intolerance prevalence was higher in patients on parenteral (20.6%) than on oral MTX (6.2%) (p?intolerance, in order to intervene timely and avoid discontinuation of an effective treatment. PMID:24345416

2013-01-01

215

Pulmonary Hypertension  

MedlinePLUS

Pulmonary hypertension (PH) is high blood pressure in the arteries to your lungs. It is a serious condition. If you have ... and you can develop heart failure. Symptoms of PH include Shortness of breath during routine activity, such ...

216

Neonatal Hypertension  

Microsoft Academic Search

\\u000a Hypertension as a clinical problem in newborn infants was first recognized in the 1970s (1). However, recent advances in our ability to identify, evaluate, and care for prmature infants have lead to an increased awareness\\u000a of neonatal hypertension, not only in the neonatal intensive care unit (NICU) but also in the neonatal follow-up clinic. This\\u000a chapter will focus on the

Joseph T. Flynn

217

Arterial Hypertension  

Microsoft Academic Search

\\u000a High blood pressure (BP) is a very important cardiovascular (CV) risk factor and is often labeled the “silent killer” because\\u000a arterial hypertension will lead to serious CV events such as ischemic heart disease, stroke, and heart failure. Moreover,\\u000a uncontrolled essential hypertension also leads to renal insufficiency, which accelerates the process of blood pressure elevation\\u000a (1, 2). There is a shift

Daniel A. Duprez

218

Exercise Intolerance in Individuals With Postconcussion Syndrome  

PubMed Central

Context: Little is known about exercise intolerance or the utility of an exercise evaluation in patients with postconcussion syndrome (PCS). Objective: To assess exercise intolerance in male and female patients with PCS. Design: Cross-sectional study. Setting: Laboratory setting. Patients or Other Participants: Participants included a convenience sample of 34 patients with PCS (17 males, 17 females; age = 25.9 ± 10.9 years) and 22 uninjured individuals on whom we gathered historical deidentified laboratory data (control group; 11 males, 11 females; age = 23.3 ± 6.2 years). Main Outcome Measure(s): Self-reported symptoms, heart rate, systolic and diastolic blood pressures (BPs), and the Borg rating of perceived exertion were measured before, during each minute of, and immediately after a graded treadmill exercise test (Balke protocol). Exercise was stopped when participants could no longer maintain the effort or reported the onset of or increase in PCS symptoms. Results: Exercise test duration (8.5 ± 4.4 minutes versus 17.9 ± 3.6 minutes; t51 = 1.8, P < .001), heart rate (142.8 ± 24.1 versus 175.2 ± 17.4; t54 = ?5.5, P < .001), and systolic BP (142.1 ± 18.3 mm Hg versus 155.5 ± 24.5 mm Hg; t53 = 2.3, P = .02) were lower, and diastolic BP (78.4 ± 10.2 mm Hg versus 73.5 ± 11.7 mm Hg; t53 = 2.2, P = .03) was higher at test cessation in the PCS than control group. Cox regression showed the odds of a shorter exercise duration were nearly 8 times greater in the PCS than control group (hazard ratio = 7.93; 95% confidence interval = 3.39, 18.56). In the general linear models that adjusted for differences in test duration, rating of perceived exertion was the only physiologic measure to show an overall difference between groups, with the control group reporting higher ratings than the PCS group (t53 = ?6.0, P < .001). Within the PCS group, systolic BP was the only measure to show a sex effect, with males showing higher pressure readings than females throughout the exercise tests (t31 = 2.8, P = .009). Conclusions: Patients with PCS had a symptom-limited response to exercise, and the treadmill test was a potentially useful tool to monitor the recovery from PCS. PMID:23952041

Kozlowski, Karl F.; Graham, James; Leddy, John J.; Devinney-Boymel, Lee; Willer, Barry S.

2013-01-01

219

Glucose Tests  

MedlinePLUS

... sample is used. Some diabetics may use a continuous glucose monitor, which uses a small sensor wire ... sample is collected. Some diabetics may use a continuous glucose monitor, which uses a small sensor wire ...

220

Systemic lactose intolerance: a new perspective on an old problem.  

PubMed

Intolerance to certain foods can cause a range of gut and systemic symptoms. The possibility that these can be caused by lactose has been missed because of "hidden" lactose added to many foods and drinks inadequately labelled, confusing diagnosis based on dietary removal of dairy foods. Two polymorphisms, C/T13910 and G/A22018, linked to hypolactasia, correlate with breath hydrogen and symptoms after lactose. This, with a 48 hour record of gut and systemic symptoms and a six hour breath hydrogen test, provides a new approach to the clinical management of lactose intolerance. The key is the prolonged effect of dietary removal of lactose. Patients diagnosed as lactose intolerant must be advised of "risk" foods, inadequately labelled, including processed meats, bread, cake mixes, soft drinks, and lagers. This review highlights the wide range of systemic symptoms caused by lactose intolerance. This has important implications for the management of irritable bowel syndrome, and for doctors of many specialties. PMID:15749792

Matthews, S B; Waud, J P; Roberts, A G; Campbell, A K

2005-03-01

221

Renal denervation in the treatment of resistant arterial hypertension.  

PubMed

Patients with resistant arterial hypertension have an increased risk of stroke, myocardial infarction, heart failure, and chronic kidney disease. In many cases, limitations of pharmacological treatment like intolerance and adherence to the antihypertensive medications are present in the clinical setting. In this context, new treatment options like trans-femoral sympathetic renal nerve denervation is, even after publication of the Symplicity HTN-3 trial, a promising new treatment option. PMID:25394989

Lambert, Thomas; Schützenberger, Wilhelm; Steinwender, Clemens

2014-12-01

222

Reference values for 75 g oral glucose tolerance test in pregnancy  

Microsoft Academic Search

A 75 g oral glucose tolerance test was performed in 212 pregnant women with no predisposing factors suggesting glucose intolerance to establish the normal pattern of glucose metabolism in pregnancy. Reference values for the test were established for the middle of pregnancy (14-20 weeks, n=43) and late pregnancy (28-37 weeks, n=168). One woman was excluded because she had diabetes that

M Hatem; F Anthony; P Hogston; D J F Rowe; K J Dennis

1988-01-01

223

Treadmill training improves intravenous glucose tolerance and insulin sensitivity in fatty zucker rats  

Microsoft Academic Search

Summary  The effect of treadmill training on intravenous glucose tolerance and insulin sensitivity was investigated in Zucker rats (fafa). In 25-week-old fafa animals with the typical metabolic syndrome of massive obesity, glucose intolerance, hypertriglyceridaemia and insulin resistance, treadmill exercise of only very mild intensity was carried out for 6 weeks. The training programme induced a marked reduction in basal and post-glucose

K. Becker-Zimmermann; M. Berger; P. Berchtold; F. A. Gries; L. Herberg; M. Schwenen

1982-01-01

224

[Hyponatremia : The water-intolerant patient].  

PubMed

Hyponatremia due to intolerance to water is a frequent clinical condition and associated with increased mortality. Besides the well known neurological symptoms, gait disturbances, falls, fractures and osteoporosis have also been described recently in patients with chronic hyponatremia. Acute hyponatremia is a more dramatic situation and needs rapid action when severe neurological symptoms are present. Hypertonic saline is recommended to treat this condition until relief of severe symptoms. The causes of hyponatremia have to be carefully examined. Especially diuretics, antidepressants and endocrine causes, e.g. hypothyroidism, hypocortisolism and hypoaldosteronism should be excluded by examination of the patient history, clinical examination and by laboratory tests. Patients should be classified as being euvolemic, hypovolemic or hypervolemic. Whereas acute hyponatremia with severe symptom should be treated with hypertonic saline, euvolemic hyponatremia due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) with mild and moderate symptoms can now be treated with tolvaptan, a selective V(2)-vasopressin antagonist. Oral tolvaptan has been shown to be an effective and potent aquaretic to treat hyponatremia caused by SIADH as evidenced by a simultaneous increase in serum sodium and a decrease in urine osmolality. The condition of patients with mild or moderate hyponatremia is also improved. Side effects associated with tolvaptan include increased thirst, dry mouth, polyuria and hypernatremia. Rapid increases in serum sodium should be avoided by close monitoring in a hospital setting. PMID:22911166

Hensen, J

2012-09-01

225

Endogenous circulating sympatholytic factor in orthostatic intolerance  

NASA Technical Reports Server (NTRS)

Sympathotonic orthostatic hypotension (SOH) is an idiopathic syndrome characterized by tachycardia, hypotension, elevated plasma norepinephrine, and symptoms of orthostatic intolerance provoked by assumption of an upright posture. We studied a woman with severe progressive SOH with blood pressure unresponsive to the pressor effects of alpha(1)-adrenergic receptor (AR) agonists. We tested the hypothesis that a circulating factor in this patient interferes with vascular adrenergic neurotransmission. Preincubation of porcine pulmonary artery vessel rings with patient plasma produced a dose-dependent inhibition of vasoconstriction to phenylephrine in vitro, abolished vasoconstriction to direct electrical stimulation, and had no effect on nonadrenergic vasoconstrictive stimuli (endothelin-1), PGF-2alpha (or KCl). Preincubation of vessels with control plasma was devoid of these effects. SOH plasma inhibited the binding of an alpha(1)-selective antagonist radioligand ([(125)I]HEAT) to membrane fractions derived from porcine pulmonary artery vessel rings, rat liver, and cell lines selectively overexpressing human ARs of the alpha(1B) subtype but not other AR subtypes (alpha(1A) and alpha(1D)). We conclude that a factor in SOH plasma can selectively and irreversibly inhibit adrenergic ligand binding to alpha(1B) ARs. We propose that this factor contributes to a novel pathogenesis for SOH in this patient. This patient's syndrome represents a new disease entity, and her plasma may provide a unique tool for probing the selective functions of alpha(1)-ARs.

Shapiro, R. E.; Winters, B.; Hales, M.; Barnett, T.; Schwinn, D. A.; Flavahan, N.; Berkowitz, D. E.

2000-01-01

226

Perceived lactose intolerance in adult Canadians: a national survey.  

PubMed

Although double-blind studies show that lactose-intolerant individuals can consume moderate quantities of milk products without perceptible symptoms, many who perceive that they are lactose intolerant limit or avoid milk products, potentially compromising calcium and vitamin D intakes. Adult Canadians are at risk of inadequate intakes of these nutrients, but no data exist on the prevalence, correlates, and potential impact of perceived lactose intolerance among Canadians. To address this, a Web-based survey of a population-representative sample of 2251 Canadians aged ?19 years was conducted. Overall, 16% self-reported lactose intolerance. This was more common in women (odds ratio (OR), 1.84; 95% CI, 1.46-2.33) and in nonwhites (OR, 1.79; 95% CI, 1.24-2.58) and less common in those >50 years of age (OR, 0.71; 95% CI, 0.56-0.90) and in those completing the survey in French (OR, 0.74; 95% CI, 0.56-0.99). Those with self-reported lactose intolerance had lower covariate-adjusted milk product and alternative intakes (mean ± SE; 1.40 ± 0.08 servings·day(-1) vs. 2.33 ± 0.03 servings·day(-1), p < 0.001). A greater proportion used supplements containing calcium (52% vs. 37%, p < 0.001) and vitamin D (58% vs. 46%, p < 0.001), but calcium intakes from the combination of milk products, alternatives, and supplements were lower (739 ± 30 mg·day(-1) vs. 893 ± 13 mg·day(-1), p < 0.0001). Variation in self-reported lactose intolerance by sex, age, and language preference was unexpected and suggests that some groups may be more vulnerable to the perception that they are lactose intolerant. Regardless of whether lactose intolerance is physiologically based or perceptual, education is required to ensure that calcium intakes are not compromised. PMID:23855270

Barr, Susan I

2013-08-01

227

Metabolic handling of orally administered glucose in cirrhosis.  

PubMed Central

We used a dual-isotope method (oral [1-14C]glucose and intravenous [6-3H]glucose) to examine whether the oral glucose intolerance of cirrhosis is due to (a) a greater input of glucose into the systemic circulation (owing to a lower first-pass hepatic uptake of ingested glucose, or to impaired inhibition of hepatic glucose output), (b) a lower rate of glucose removal, or (c) a combination of these mechanisms. Indirect calorimetry was used to measure oxidative and nonoxidative metabolism. Basal plasma glucose levels (cirrhotics, 5.6 +/- 0.4[SE], controls, 5.1 +/- 0.2 mmol/liter), and rates of glucose appearance (Ra) and disappearance (Rd) were similar in the two groups. After 75 g of oral glucose, plasma glucose levels were higher in cirrhotics than controls, the curves diverging for 80 min despite markedly higher insulin levels in cirrhotics. During the first 20 min, there was very little change in glucose Rd and the greater initial increase in plasma glucose in cirrhotics resulted from a higher Ra of ingested [1-14C]glucose into the systemic circulation, suggesting a reduced first-pass hepatic uptake of portal venous glucose. The continuing divergence of the plasma glucose curves was due to a lower glucose Rd between 30 and 80 min (cirrhotics 236 +/- 17 mg/kg in 50 min, controls 280 +/- 17 mg/kg in 50 min, P < 0.05, one-tailed test). Glucose metabolic clearance rate rose more slowly in cirrhotics and was significantly lower than in controls during the first 2 h after glucose ingestion (2.24 +/- 0.17 vs 3.30 +/- 0.23 ml/kg per min, P < 0.005), in keeping with their known insulin insensitivity. Despite the higher initial glucose Ra in cirrhotics, during the entire 4-h period the quantity of total glucose and of ingested glucose (cirrhotics 54 +/- 2 g [72% of oral load], controls 54 +/- 3 g) appearing in the systemic circulation were similar. Overall glucose Rd (cirrhotics 72.5 +/- 3.8 g/4 h, controls 77.2 +/- 2.2 g/4h) and percent suppression of hepatic glucose output over 4 h (cirrhotics, 53 +/- 10%, controls 49 +/- 8%) were also similar. After glucose ingestion much of the extra glucose utilized was oxidized to provide energy that in the basal state was derived from lipid fuels. Glucose oxidation after glucose ingestion was similar in both groups and accounted for approximately two-thirds of glucose Rd. The reduction in overall nonoxidative glucose disposal did not reach significance (21 +/- 5 vs. 29 +/- 3 g/4 h, 0.05 < P < 0.1). Although our data would be compatible with an impairment of tissue glycogen deposition after oral glucose, glucose storage as glycogen probably plays a small part part in overall glucose disposal. Our results suggest that the higher glucose levels seen in cirrhotics after oral glucose are due initially to an increase in the amount of ingested glucose appearing in the systemic circulation, and subsequently to an impairment in glucose uptake by tissues due to insulin insensitivity. Impaired suppression of hepatic glucose output does not contribute to oral glucose intolerance. PMID:8450036

Kruszynska, Y T; Meyer-Alber, A; Darakhshan, F; Home, P D; McIntyre, N

1993-01-01

228

NMR measurements of intracellular ions in hypertension  

NASA Astrophysics Data System (ADS)

The NMR methods for the measurement of intracellular free Na+, K+, Mg2+, Ca2+, and H+ are introduced. The recent literature is then presented showing applications of these methods to cells and tissues from hypertensive animal model systems, and humans with essential hypertension. The results support the hypothesis of consistent derangement of the intracellular ionic environment in hypertension. The theory that this derangement may be a common link in the disease states of high blood pressure and abnormal insulin and glucose metabolism, which are often associated clinically, is discussed.

Veniero, Joseph C.; Gupta, R. K.

1993-08-01

229

Fructose transporters GLUT5 and GLUT2 expression in adult patients with fructose intolerance  

PubMed Central

Background Gastrointestinal symptoms and malabsorption following fructose ingestion (fructose intolerance) are common in functional gastrointestinal disorders (FGID). The underlying mechanism is unclear, but is hypothesized to be related an abnormality of intestinal fructose transporter proteins. Objective To assess the expression of the main intestinal fructose transporter proteins, glucose transport protein 5 (GLUT5) and 2 (GLUT2), in FGID. Methods The expression of GLUT5 and GLUT2 protein and mRNA in small intestinal biopsy tissue was investigated using real-time reverse-transcription PCR and Western immunoblotting in 11 adults with FGID and fructose intolerance ascertained by breath testing and in 15 controls. Results Median expression levels of GLUT5 mRNA normalized to beta-actin were 0.18 (interquartile range, IQR, 0.13–0.21) in patients and 0.17 (IQR 0.12–0.19) in controls (p?>?0.05). Respective levels of GLUT2 mRNA were 0.26 (IQR 0.20–0.31) and 0.26 (IQR 0.19–0.31) (p?>?0.05). Median expression levels of GLUT5 protein normalized to alpha-tubulin were 0.95 (IQR 0.52–1.68) in patients and 0.95 (IQR 0.59–1.15) in controls (p?>?0.05). Respective protein expression levels for GLUT2 were 1.56 (IQR 1.06–2.14) and 1.35 (IQR 0.96–1.79) (p?>?0.05). Conclusions Human fructose intolerance may not be associated with marked changes in GLUT5 and GLUT2 expression. Replication of these results in a larger subject group, including measures of transporter activation and membrane and subcellular localization, is warranted. PMID:24918004

Li, Xinhua; Ho, Sherry SY; Leong, Sai Mun; Wong, Reuben K; Koay, Evelyn SC; Ferraris, Ronaldo P

2014-01-01

230

Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment.  

PubMed

Lactose malabsorption is a common condition caused by reduced expression or activity of lactase in the small intestine. In such patients, lactose intolerance is characterized by abdominal symptoms (e.g. nausea, bloating, and pain) after ingestion of dairy products. The genetic basis of lactose malabsorption is established and several tests for this condition are available, including genetic, endoscopic, and H2-breath tests. In contrast, lactose intolerance is less well understood. Recent studies show that the risk of symptoms after lactose ingestion depends on the dose of lactose, lactase expression, intestinal flora, and sensitivity of the gastrointestinal tract. Lactose intolerance has recently been defined as symptoms developing after ingestion of lactose which do not develop after placebo challenge in a person with lactose maldigestion. Such blinded testing might be especially important in those with functional gastrointestinal diseases in whom self-reported lactose intolerance is common. However, placebo-controlled testing is not part of current clinical practice. Updated protocols and high-quality outcome studies are needed. Treatment options of lactose intolerance include lactose-reduced diet and enzyme replacement. Documenting the response to multiple doses can guide rational dietary management; however, the clinical utility of this strategy has not been tested. This review summarizes the genetic basis, diagnosis, and treatment of lactose malabsorption and intolerance. PMID:24917953

Misselwitz, Benjamin; Pohl, Daniel; Frühauf, Heiko; Fried, Michael; Vavricka, Stephan R; Fox, Mark

2013-06-01

231

Lactose malabsorption and intolerance: pathogenesis, diagnosis and treatment  

PubMed Central

Lactose malabsorption is a common condition caused by reduced expression or activity of lactase in the small intestine. In such patients, lactose intolerance is characterized by abdominal symptoms (e.g. nausea, bloating, and pain) after ingestion of dairy products. The genetic basis of lactose malabsorption is established and several tests for this condition are available, including genetic, endoscopic, and H2-breath tests. In contrast, lactose intolerance is less well understood. Recent studies show that the risk of symptoms after lactose ingestion depends on the dose of lactose, lactase expression, intestinal flora, and sensitivity of the gastrointestinal tract. Lactose intolerance has recently been defined as symptoms developing after ingestion of lactose which do not develop after placebo challenge in a person with lactose maldigestion. Such blinded testing might be especially important in those with functional gastrointestinal diseases in whom self-reported lactose intolerance is common. However, placebo-controlled testing is not part of current clinical practice. Updated protocols and high-quality outcome studies are needed. Treatment options of lactose intolerance include lactose-reduced diet and enzyme replacement. Documenting the response to multiple doses can guide rational dietary management; however, the clinical utility of this strategy has not been tested. This review summarizes the genetic basis, diagnosis, and treatment of lactose malabsorption and intolerance. PMID:24917953

Pohl, Daniel; Frühauf, Heiko; Fried, Michael; Vavricka, Stephan R; Fox, Mark

2013-01-01

232

Visceral hypersensitivity and intolerance symptoms in lactose malabsorption.  

PubMed

Lactose malabsorption is not always associated with intolerance symptoms. The factors responsible for symptom onset are not yet completely known. As differences in visceral sensitivity may play a role in the pathogenesis of functional symptoms, we evaluated whether an alteration of visceral sensitivity is present in subjects with lactose intolerance. Thirty subjects, recruited regardless of whether they were aware of their capacity to absorb lactose, underwent an evaluation of intestinal hydrogen production capacity by lactulose breath test, followed by an evaluation of lactose absorption by hydrogen breath test after lactose administration and subsequently an evaluation of recto-sigmoid sensitivity threshold during fasting and after lactulose administration, to ascertain whether fermentation modifies intestinal sensitivity. The role of differences in gastrointestinal transit was excluded by gastric emptying and mouth-to-caecum transit time by (13)C-octanoic and lactulose breath tests. Lactulose administration induced a significant reduction of discomfort threshold in subjects with lactose intolerance but not in malabsorbers without intolerance symptoms or in subjects with normal lactose absorption. Perception threshold showed no changes after lactulose administration. Severity of symptoms in intolerant subjects was significantly correlated with the reduction of discomfort thresholds. Visceral hypersensitivity should be considered in the induction of intolerance symptoms in subjects with lactose malabsorption. PMID:17973635

Di Stefano, M; Miceli, E; Mazzocchi, S; Tana, P; Moroni, F; Corazza, G R

2007-11-01

233

Glucose tolerance, insulin release, and insulin binding to monocytes in kidney transplant recipients  

SciTech Connect

In order to evaluate glucose tolerance following renal transplantation, intravenous glucose tolerance tests (IVGTT), with evaluation of hormonal responses to the intravenous glucose load and percent specific /sup 125/I-insulin binding to peripheral blood monocytes, were studied in eight clinically stable kidney transplant recipients. For comparison purposes, identical studies were done in eight control subjects and seven clinically stable hemodialysis patients. One transplant recipient was glucose intolerant, with fasting hyperglycemia, elevated HbA1C, and abnormal glucose decay constant. Impaired pancreatic insulin release appeared to be the major factor accounting for his glucose intolerance. The seven glucose-tolerant transplant recipients had significantly increased insulin release during IVGTT compared to control subjects, and significant correlations were found among insulin release, glucose decay constant, and fasting blood sugar in those patients. Insulin binding to monocytes was significantly greater in transplant recipients than control subjects due to an increase in insulin binding capacity per cell. A significant correlation was found between percent specific /sup 125/I-insulin binding and steroid dose, expressed as mg/kg body weight/day, in those patients. Thus, chronic steroid administration does not cause glucose intolerance in transplant recipients who manifest steroid-associated increases in pancreatic insulin release and cellular insulin binding capacity.

Briggs, W.A.; Wielechowski, K.S.; Mahajan, S.K.; Migdal, S.D.; McDonald, F.D.

1982-03-01

234

[Portopulmonary hypertension].  

PubMed

Patients with portal hypertension may develop pulmonary complications such as hepatopulmonary syndrome (HPS) or portopulmonary hypertension (PPHT). PPHT is defined as elevated pulmonary pressure, elevated pulmonary vascular resistance, a normal pulmonary capillary wedge pressure, and portal hypertension in the absence of other known causes pulmonary hypertension. Various factors such as hyperdynamic circulation, volume overload, and circulating vasoactive mediators are suspected to be involved in the pathogenesis of PPHT. The prognosis of patients with severe PPHT is significantly reduced due to the risk of right heart failure. In patients with moderate to severe PPHT liver transplantation is associated with a significantly increased mortality. The chief symptom of PPHT may be dyspnoe in the presence of typical histomorphological alterations comparable with idiopathic pulmonary hypertension. Continuous intravenous application of prostacyclin is currently regarded as the treatment of choice for patients with severe PPHT. Inhaled prostacyclin or its analogue iloprost or oral treatment with the endothelin-receptor antagonist bosentan may be promising alternatives which should be further investigated in randomized controlled trials. PMID:16001350

Halank, M; Miehlke, S; Kolditz, M; Hoeffken, G

2005-07-01

235

Effect of a late evening snack on the blood glucose level and energy metabolism in patients with liver cirrhosis  

Microsoft Academic Search

Background\\/aim: Patients with liver cirrhosis suffer from energy malnutrition. Late evening snacks (LESs) have been recently reported to be effective for this. However, it is known that a significant proportion of patients with liver cirrhosis have glucose intolerance as a complication. For this reason, the influence of LES on the blood glucose level should be examined. Subjects\\/method: We administered an

Mariko Okamoto; Isao Sakaida; Masako Tsuchiya; Chieko Suzuki; Kiwamu Okita

2003-01-01

236

Influence of Maternal Plane of Nutrition and Arginine Supplementation on Mares and Their Foals: Glucose and Insulin Dynamics  

E-print Network

effect on intrauterine environment. Adaptations to maternal nutrition can alter maternal metabolism, and eventually, impact fetal growth and development through influence of the intrauterine environment. The intrauterine environment directly...). 9 The intrauterine programming of fetal metabolism occurs during late gestation as pancreatic insulin production begins to respond to available glucose (Fowden and Hill, 2001; Fowden et al., 2005). Glucose intolerance and other metabolic...

Hanson, Andrea

2012-10-19

237

Improvement of diabetes, obesity and hypertension in type 2 diabetic KKA{sup y} mice by bis(allixinato)oxovanadium(IV) complex  

SciTech Connect

Previously, we found that bis(allixinato)oxovanadium(IV) (VO(alx){sub 2}) exhibits a potent hypoglycemic activity in type 1-like diabetic mice. Since the enhancement of insulin sensitivity is involved in one of the mechanisms by which vanadium exerts its anti-diabetic effects, VO(alx){sub 2} was further tested in type 2 diabetes with low insulin sensitivity. The effect of oral administration of VO(alx){sub 2} was examined in obesity-linked type 2 diabetic KKA{sup y} mice. Treatment of VO(alx){sub 2} for 4 weeks normalized hyperglycemia, glucose intolerance, hyperinsulinemia, hypercholesterolemia and hypertension in KKA{sup y} mice; however, it had no effect on hypoadiponectinemia. VO(alx){sub 2} also improved hyperleptinemia, following attenuation of obesity in KKA{sup y} mice. This is the first example in which a vanadium compound improved leptin resistance in type 2 diabetes by oral administration. On the basis of these results, VO(alx){sub 2} is proposed to enhance not only insulin sensitivity but also leptin sensitivity, which in turn improves diabetes, obesity and hypertension in an obesity-linked type 2 diabetic animal.

Adachi, Yusuke [Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, 5 Nakauchi-cho, Misasagi, Yamashina-ku, Kyoto 607-8414 (Japan); Yoshikawa, Yutaka [Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, 5 Nakauchi-cho, Misasagi, Yamashina-ku, Kyoto 607-8414 (Japan); Yoshida, Jiro [Healthcare Institute, Wakunaga Pharmaceutical Co. Ltd, 1624 Shimokotachi, Koda-cho, Takatagun, Hiroshima 739-1195 (Japan); Kodera, Yukihiro [Healthcare Institute, Wakunaga Pharmaceutical Co. Ltd, 1624 Shimokotachi, Koda-cho, Takatagun, Hiroshima 739-1195 (Japan)]. E-mail: kodera_y@wakunaga.co.jp; Katoh, Akira [Department of Materials and Life Science, Faculty of Science and Technology, Seikei University, 3-3-1 Kitamachi, Kichijoji, Musashino-shi, Tokyo 180-8633 (Japan)]. E-mail: katoh@st.seikei.ac.jp; Takada, Jitsuya [Research Reactor Institute, Kyoto University, Osaka 590-0494 (Japan)]. E-mail: takada@hl.rri.kyoto-u.ac.jp; Sakurai, Hiromu [Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, 5 Nakauchi-cho, Misasagi, Yamashina-ku, Kyoto 607-8414 (Japan)]. E-mail: sakurai@mb.kyoto-phu.ac.jp

2006-07-07

238

Glucose metabolic gene expression in growth hormone transgenic coho salmon.  

PubMed

Salmonids are generally known to be glucose intolerant. However, previous studies have shown that growth hormone (GH) transgenic coho salmon display modified nutritional regulation of glycolysis and lipogenesis compared to non-transgenic fish, suggesting the potential for better use of glucose in GH transgenic fish. To examine this in detail, GH transgenic and non-transgenic coho salmon were subjected to glucose tolerance test and subsequent metabolic assessments. After intra-peritoneal injection of 250mg/kg glucose, we analysed post-injection kinetics of glycaemia and expression of several key target genes highly involved in glucose homeostasis in muscle and liver tissues. Our data show no significant differences in plasma glucose levels during peak hyperglycaemia (3-6h after injection), demonstrating a similar glucose tolerance between transgenic and non transgenic. However, and unrelated to the hyperglycaemic episode, GH transgenic fish return to a slightly lower basal glycaemia values 24h after injection. Correspondingly, GH transgenic fish exhibited higher mRNA levels of glucokinase (GK) and glucose-6-phosphate dehydrogenase (G6PDH) in liver, and glucose transporter (GLUT4) in muscle. These data suggest that these metabolic actors may be involved in different glucose use in GH transgenic fish, which would be expected to influence the glucose challenge response. Overall, our data demonstrate that GH transgenic coho salmon may be a pertinent animal model for further study of glucose metabolism in carnivorous fish. PMID:24486143

Panserat, Stéphane; Kamalam, Biju Sam; Fournier, Jeanne; Plagnes-Juan, Elisabeth; Woodward, Krista; Devlin, Robert H

2014-04-01

239

Assessing Cell K Physiology in Hypertensive Patients  

Microsoft Academic Search

The assessment of potassium (K) effects in hypertension involves a history of complex research in cell K function and body K homeostasis. These studies provide evidence for the role of K ions in vascular and renal function, insulin resistance, glucose uptake, and the renin–angiotensin–aldosterone system; and there have been an impressive number of clinical and epidemiologic research relating dietary intake

Antonio Delgado-Almeida

2006-01-01

240

Food Allergy and Intolerance: Diagnoses and Nutritional Management  

Microsoft Academic Search

\\u000a \\u000a \\u000a \\u000a \\u000a \\u000a • \\u000a \\u000a \\u000a Adverse food reactions (hypersensitivity) can be either immune mediated (food allergy) or nonimmune mediated (intolerance).\\u000a \\u000a \\u000a \\u000a • \\u000a \\u000a \\u000a Nonimmune mediated reactions (intolerance) are classified as enzymatic, pharmacologic, or undefined food intolerance; together\\u000a they account for the majority of food hypersensitivity reactions.\\u000a \\u000a \\u000a \\u000a \\u000a • \\u000a \\u000a \\u000a Diagnosis of food allergy is based on medical history, physical examination, and diagnostic tests; the oral food challenge\\u000a is

Kathy Roberts

241

Sodium Oxybate Intolerance Associated with Familial Serum Acylcarnitine Elevation  

PubMed Central

Our case describes clinical features of two families defined by joint phenotypes: sodium oxybate intolerance and elevated serum acylcarnitines. Oxybate intolerance variably presents as either cervical dystonia or sleep-related eating disorder. Our objective is to identify biological markers which predict a poor response to sodium oxybate as a treatment for disturbed sleep. Familial inheritance pattern, genotype analysis, multiorgan system involvement, and response to treatment suggest the presence of a secondary cause of fatty oxidation defect, i.e., mitochondrial disorder. Our case report supports the possible conclusion that variance in human mitochondrial metabolism may affect sodium oxybate tolerability. Citation: Berner J. Sodium oxybate intolerance associated with familial serum acylcarnitine elevation. J Clin Sleep Med 2013;9(1):71-72. PMID:23319908

Berner, Jon

2013-01-01

242

Towards an ontological theory of substance intolerance and hypersensitivity.  

PubMed

A proper ontological treatment of intolerance--including hypersensitivity--to various substances is critical to patient care and research. However, existing methods and standards for documenting these conditions have flaws that inhibit these goals, especially translational research that bridges the two activities. In response, I outline a realist approach to the ontology of substance intolerance, including hypersensitivity conditions. I defend a view of these conditions as a subtype of disease. Specifically, a substance intolerance is a disease whose pathological process(es) are realized upon exposure to a quantity of substance of a particular type, and this quantity would normally not cause the realization of the pathological process(es). To develop this theory, it was necessary to build pieces of a theory of pathological processes. Overall, however, the framework of the Ontology for General Medical Science (which uses Basic Formal Ontology as its uppermost level) was a more-than-adequate foundation on which to build the theory. PMID:20152933

Hogan, William R

2011-02-01

243

[Lactose intolerance: changing paradigms due to molecular biology].  

PubMed

In most mammals, lactase activity declines on the intestinal wall after weaning, characterizing primary hypolactasia that provokes symptoms of lactose intolerance. The intensity of symptoms of distention, flatulence, abdominal pain and diarrhea varies, according to the amount of ingested lactose, and increases with age. Hypolactasia is genetically determined; nonetheless, a mutation occurred that had made a part of mankind tolerate milk in adulthood. Diagnosis is made by a tolerance test, using the lactose challenge. With the discovery made by the Finns of polymorphism associated with lactase persistence, mainly, in Northern Europe, the genetic test was incorporated as a more comfortable diagnostic tool for the intolerant. In Brazil, 43% of Caucasian and Mulatto groups have lactase persistence allele, with hipolactasia more frequently found among Blacks and Japanese. However, in clinical practice people with hypolactasia may be advised to consume certain dairy products and food containing lactose without developing intolerance symptoms, whereas others will need a lactose restriction diet. PMID:20499001

Mattar, Rejane; Mazo, Daniel Ferraz de Campos

2010-01-01

244

Dairy Intake, Dietary Adequacy, and Lactose Intolerance12  

PubMed Central

Despite repeated emphasis in the Dietary Guidelines for Americans on the importance of calcium in the adult American diet and the recommendation to consume 3 dairy servings a day, dairy intake remains well below recommendations. Insufficient health professional awareness of the benefits of calcium and concern for lactose intolerance are among several possible reasons, This mini-review highlights both the role of calcium (and of dairy, its principal source in modern diets) in health maintenance and reviews the means for overcoming lactose intolerance (real or perceived). PMID:23493531

Heaney, Robert P.

2013-01-01

245

Sodium oxybate intolerance associated with familial serum acylcarnitine elevation.  

PubMed

Our case describes clinical features of two families defined by joint phenotypes: sodium oxybate intolerance and elevated serum acylcarnitines. Oxybate intolerance variably presents as either cervical dystonia or sleep-related eating disorder. Our objective is to identify biological markers which predict a poor response to sodium oxybate as a treatment for disturbed sleep. Familial inheritance pattern, genotype analysis, multiorgan system involvement, and response to treatment suggest the presence of a secondary cause of fatty oxidation defect, i.e., mitochondrial disorder. Our case report supports the possible conclusion that variance in human mitochondrial metabolism may affect sodium oxybate tolerability. PMID:23319908

Berner, Jon

2013-01-15

246

The forgotten role of glucose effectiveness in the regulation of glucose tolerance.  

PubMed

Glucose effectiveness (S G) is the ability of glucose per se to stimulate its own uptake and to suppress its own production under basal/constant insulin concentrations. In an individual, glucose tolerance is a function of insulin secretion, insulin action and S G. Under conditions of declining insulin secretion and action (e.g. type 2 diabetes), the degree of S G assumes increasing significance in determining the level of glucose tolerance both in fasted and postprandial states. Although the importance of S G has been recognized for years, mechanisms that contribute to S G are poorly understood. Research data on modulation of S G and its impact in glucose intolerance is limited. In this review, we will focus on the role of S G in the regulation of glucose tolerance, its evaluation, and potential advantages of therapies that can enhance glucose-induced stimulation of glucose uptake and suppression of its own production in conditions of impaired insulin secretion and action. PMID:25869240

Dube, Simmi; Errazuriz-Cruzat, Isabel; Basu, Ananda; Basu, Rita

2015-06-01

247

Clinical role of a fixed combination of standardized Berberis aristata and Silybum marianum extracts in diabetic and hypercholesterolemic patients intolerant to statins  

PubMed Central

Background Statin intolerance is a medical condition often leading patients to nonadherence to the prescribed therapy or to a relevant reduction of the statin dosage. Both situations determine a totally or partially uncontrolled lipid profile, and these conditions unquestionably increase the risk of cardiovascular events. Methods We enrolled hypercholesterolemic, type 2 diabetic patients complaining of intolerance to statins. Some of them had reduced the statin dose ‘until the disappearance of symptoms’; others had opted for treatment with ezetimibe; and yet others were not undergoing any treatment at all. All patients of the three groups were then given a fixed combination of berberine and silymarin (Berberol®), known from previous papers to be able to control both lipidic and glycemic profiles. Results The tested product both as a single therapy and as add-on therapy to low-dose statin or to ezetimibe reduced triglycerides, low-density lipoprotein cholesterol, fasting blood glucose, and glycosylated hemoglobin in a significant manner without inducing toxicity conditions that might be somehow ascribed to a statin-intolerant condition. Conclusion Our study demonstrates that use of Berberol®, administered as a single or add-on therapy in statin-intolerant subjects affected by diabetes and hypercholesterolemia is a safe and effective tool capable of improving the patients’ lipidic and glycemic profiles. PMID:25678808

Di Pierro, Francesco; Bellone, Iaele; Rapacioli, Giuliana; Putignano, Pietro

2015-01-01

248

Hormones and Hypertension  

MedlinePLUS

... blood pressure increases with age. DiD you know? Primary hypertension (high blood pressure) most often can be controlled ... key role in the start and continuation of primary hypertension. Secondary hypertension is due to other diseases such ...

249

Preliminary Investigation of Intolerance of Uncertainty Treatment for Anxiety Disorders  

ERIC Educational Resources Information Center

Intolerance of uncertainty (IU) is the tendency to react negatively to uncertain situations or events, and it has been found to be an important maintaining factor in a number of different anxiety disorders. It is often included as a part of cognitive behavioural interventions for anxiety disorders but its specific contribution to treatment outcome…

Hewitt, Sarah N.; Egan, Sarah; Rees, Clare

2009-01-01

250

Are ambiguity aversion and ambiguity intolerance identical? A neuroeconomics investigation  

PubMed Central

In recent years, there has been growing interest in understanding a person's reaction to ambiguous situations, and two similar constructs related to ambiguity, “ambiguity aversion” and “ambiguity intolerance,” are defined in different disciplines. In the field of economic decision-making research, “ambiguity aversion” represents a preference for known risks relative to unknown risks. On the other hand, in clinical psychology, “ambiguity intolerance” describes the tendency to perceive ambiguous situations as undesirable. However, it remains unclear whether these two notions derived from different disciplines are identical or not. To clarify this issue, we combined an economic task, psychological questionnaires, and voxel-based morphometry (VBM) of structural brain magnetic resonance imaging (MRI) in a sample of healthy volunteers. The individual ambiguity aversion tendency parameter, as measured by our economic task, was negatively correlated with agreeableness scores on the self-reported version of the Revised NEO Personality Inventory. However, it was not correlated with scores of discomfort with ambiguity, one of the subscales of the Need for Closure Scale. Furthermore, the ambiguity aversion tendency parameter was negatively correlated with gray matter (GM) volume of areas in the lateral prefrontal cortex and parietal cortex, whereas ambiguity intolerance was not correlated with GM volume in any region. Our results suggest that ambiguity aversion, described in decision theory, may not necessarily be identical to ambiguity intolerance, referred to in clinical psychology. Cautious applications of decision theory to clinical neuropsychiatry are recommended. PMID:25698984

Tanaka, Yusuke; Fujino, Junya; Ideno, Takashi; Okubo, Shigetaka; Takemura, Kazuhisa; Miyata, Jun; Kawada, Ryosaku; Fujimoto, Shinsuke; Kubota, Manabu; Sasamoto, Akihiko; Hirose, Kimito; Takeuchi, Hideaki; Fukuyama, Hidenao; Murai, Toshiya; Takahashi, Hidehiko

2015-01-01

251

Tolerance of Intolerance: Values and Virtues at Stake in Education  

ERIC Educational Resources Information Center

The article addresses the issue of the tolerance of intolerance in an educational context. It concerns a real case in a Swedish upper secondary school some years ago, when a student was suspended from school owing to his sympathies with Nazi ideas. One hundred and twenty student teachers' responses to this decision were analysed in respect of the…

Orlenius, Kennert

2008-01-01

252

The role of colonic microbiota in lactose intolerance.  

PubMed

In a previous study we observed a clear difference in lactose intolerance symptoms after a 25-g lactose load in two groups of persons with lactase nonpersistence and similar small intestinal lactase activity. From this observation we hypothesized a colon resistance factor. To identify this factor, the microbial composition of fecal samples of the two lactose intolerant groups (one with mild symptoms, n = 16, and one with diarrhea-predominant symptoms, n = 11) was compared using the fluorescent in situ hybridization technique. Large interindividual differences were found in the numbers of total bacteria and main groups of bacteria (CV: 0.65 and 0.64-0.82 respectively). The bacterial numbers were not significantly different between the two groups. A significant negative correlation, however, was found between the individual symptom scores of the intolerant persons and the numbers of total hybridizable bacteria (r(s) = -0.42, P = 0.03). The results suggest that an increased number of bacteria might contribute--by means of a higher fermentative capacity--to the reduction of lactose intolerance symptoms. PMID:14992439

Zhong, Yan; Priebe, Marion G; Vonk, Roel J; Huang, Cheng-Yu; Antoine, Jean-Michel; He, Tao; Harmsen, Hermie J M; Welling, Gjalt W

2004-01-01

253

Continuous Glucose Monitoring  

MedlinePLUS

... List of Topics and Titles : Continuous Glucose Monitoring Continuous Glucose Monitoring On this page: What is glucose ... upper arm, forearm, or thigh. [ Top ] What is continuous glucose monitoring? Continuous glucose monitoring (CGM) systems use ...

254

Calorie restriction initiated at middle age improved glucose tolerance without affecting age-related impairments of insulin signaling in rat skeletal muscle  

Microsoft Academic Search

Calorie restriction (CR) may affect glucose tolerance via modulation of the insulin action in skeletal muscle. The present study investigated the effect of CR initiated at middle age in rats bearing glucose intolerance, in comparison with CR at a younger age. Male F344 rats at 2.5 and 18months (mo) of age were fed ad libitum (AL) or 30% CR diets

Toshimitsu Komatsu; Hiroko Hayashi; Haruyoshi Yamaza; Takuya Chiba; Yoshikazu Higami; Kazunao Kuramoto; Isao Shimokawa

2006-01-01

255

The effects of combined vitamin D and calcium supplementation on fasting plasma glucose in non-diabetic adults age 65 and older  

Technology Transfer Automated Retrieval System (TEKTRAN)

Altered vitamin D and calcium homeostasis may play a role in the development of glucose intolerance. In a 3-year randomized controlled trial, we compared the effects of combined vitamin D and calcium supplementation vs. placebo on fasting plasma glucose (FPG) in healthy adults 65 years of age or old...

256

Plasma glucose levels as predictors of diabetes: the Mexico City diabetes study  

Microsoft Academic Search

Aims\\/hypothesis  The value of diagnostic categories of glucose intolerance for predicting type 2 diabetes is much debated. We therefore sought\\u000a to estimate relative and population-attributable risk of different definitions based on fasting (impaired fasting glucose\\u000a [IFG]) or 2 h plasma glucose concentrations (impaired glucose tolerance [IGT]) and to describe the associated clinical phenotypes.\\u000a \\u000a \\u000a \\u000a Methods  We prospectively observed a population-based cohort of 1,963 non-diabetic

E. Ferrannini; M. Massari; M. Nannipieri; A. Natali; R. Lopez Ridaura; C. Gonzales-Villalpando

2009-01-01

257

Hypertension promotes islet morphological changes with vascular injury on pre-diabetic status in SHRsp rats.  

PubMed

Abstract Hypertensive patients have a higher incidence of new-onset diabetic mellitus than normotensive subjects, and we hypothesized that hypertension induces morphological changes in islets via vascular injury. To test our hypothesis, we administrated hydralazine or irbesartan to spontaneously hypertensive stroke-prone (SHRsp) rats. A greater islet fibrosis was observed in SHRsp rats compared with controls, and irbesartan significantly ameliorated the fibrosis. High fat diet induced glucose intorelance in SHRsp rats and irbesartan but not hydralazine improved glucose torelance. We demonstrate islet morphological changes in hypertensive rats, and our data suggest that angiotensin receptor blockers have the potential to prevent islet injury. PMID:23786428

Satoh, Minoru; Nagasu, Hajime; Haruna, Yoshisuke; Ihoriya, Chieko; Kadoya, Hiroyuki; Sasaki, Tamaki; Kashihara, Naoki

2014-01-01

258

Late evening snack and the change of blood glucose level in patients with liver cirrhosis  

Microsoft Academic Search

It has been reported that patients with liver cirrhosis suffer from energy malnutrition and late evening snacks (LES) can be effective for this malnutrition. On the other hand, it is also known that some patients with liver cirrhosis have glucose intolerance as a complication. We have shown that 1 week LES treatment using as an oral supplement with branched chain

Isao Sakaida; Masako Tsuchiya; Mariko Okamoto; Kiwamu Okita

2004-01-01

259

The Relationship between Impaired Glucose Tolerance, Type 2 Diabetes, and Cognitive Function  

Microsoft Academic Search

The present review integrates findings of published studies that have evaluated the cognitive function of treated and untreated type 2 diabetic patients and provides a detailed overview of the neuropsychological assessments conducted. Cognitive deficits are observed in older people with glucose intolerance or untreated diabetes but these deficits appear to be attenuated by treatments that improve glycemic control. Cognitive decrements

Nesrine Awad; Michèle Gagnon; Claude Messier

2004-01-01

260

Rictor/mTORC2 facilitates central regulation of energy and glucose homeostasis  

PubMed Central

Insulin signaling in the central nervous system (CNS) regulates energy balance and peripheral glucose homeostasis. Rictor is a key regulatory/structural subunit of the mTORC2 complex and is required for hydrophobic motif site phosphorylation of Akt at serine 473. To examine the contribution of neuronal Rictor/mTORC2 signaling to CNS regulation of energy and glucose homeostasis, we utilized Cre-LoxP technology to generate mice lacking Rictor in all neurons, or in either POMC or AgRP expressing neurons. Rictor deletion in all neurons led to increased fat mass and adiposity, glucose intolerance and behavioral leptin resistance. Disrupting Rictor in POMC neurons also caused obesity and hyperphagia, fasting hyperglycemia and pronounced glucose intolerance. AgRP neuron specific deletion did not impact energy balance but led to mild glucose intolerance. Collectively, we show that Rictor/mTORC2 signaling, especially in POMC-expressing neurons, is important for central regulation of energy and glucose homeostasis. PMID:24944899

Kocalis, Heidi E.; Hagan, Scott L.; George, Leena; Turney, Maxine K.; Siuta, Michael A.; Laryea, Gloria N.; Morris, Lindsey C.; Muglia, Louis J.; Printz, Richard L.; Stanwood, Gregg D.; Niswender, Kevin D.

2014-01-01

261

Glucose Variability  

PubMed Central

The proposed contribution of glucose variability to the development of the complications of diabetes beyond that of glycemic exposure is supported by reports that oxidative stress, the putative mediator of such complications, is greater for intermittent as opposed to sustained hyperglycemia. Variability of glycemia in ambulatory conditions defined as the deviation from steady state is a phenomenon of normal physiology. Comprehensive recording of glycemia is required for the generation of any measurement of glucose variability. To avoid distortion of variability to that of glycemic exposure, its calculation should be devoid of a time component. PMID:23613565

2013-01-01

262

Glutathionylation of hepatic and visceral adipose proteins decreases in obese-prone, glucose intolerant rats  

Technology Transfer Automated Retrieval System (TEKTRAN)

Obesity and insulin resistance are associated with increases in oxidative stress and lipid peroxidation. On the other hand, adipocytes from obese animals have elevated GSH content, and insulin resistance can be reversed by GSH depletion. Oxidation of active site cysteines of protein tyrosine phospha...

263

Glucose intolerance in the West African Diaspora: a skeletal muscle fibre type distribution hypothesis.  

PubMed

In the United States, Black Americans are largely descendants of West African slaves; they have a higher relative proportion of obesity and experience a higher prevalence of diabetes than White Americans. However, obesity rates alone cannot explain the higher prevalence of type 2 diabetes. Type 2 diabetes is characterized by insulin resistance and beta-cell dysfunction. We hypothesize that the higher prevalence of type 2 diabetes in African Americans (as compared to White Americans) is facilitated by an inherited higher percentage of skeletal muscle fibre type II and a lower percentage of skeletal muscle fibre type I. Skeletal muscle fibre type II is less oxidative and more glycolytic than skeletal muscle fibre type I. Lower oxidative capacity is associated with lower fat oxidation and a higher disposal of lipids, which are stored as muscular adipose tissue in higher amounts in Black compared to White Americans. In physically active individuals, the influence of muscle fibre composition will not be as detrimental as in physically inactive individuals. This discrepancy is caused by the plasticity in the skeletal muscle fibre characteristics towards a higher activity of oxidative enzymes as a consequence of physical activity. We suggest that a higher percentage of skeletal muscle fibre type II combined with physical inactivity has an impact on insulin sensitivity and high prevalence of type 2 diabetes in Blacks of West African ancestry. PMID:21382179

Nielsen, J; Christensen, D L

2011-08-01

264

Oxidative stress and antioxidant status in elderly diabetes mellitus and glucose intolerance patients  

Microsoft Academic Search

Increased oxidative stress and impaired anti-oxidant defense have been suggested as contributory factors for initiation and progression of complications in diabetes mellitus. Aging itself has been shown to be along with increased oxidative stress and lower anti-oxidant defense. We aimed at investigating oxidative stress and anti-oxidant enzymes in 61 elderly subjects. Fifteen healthy individuals (group 1, mean age 72.2 ±

Teslime Atli; Kenan Keven; Aslihan Avci; Sim Kutlay; Nuran Turkcapar; Murat Varli; Sevgi Aras; Ergun Ertug; Orhan Canbolat

2004-01-01

265

Efficacy of 12-month treatment with the GH receptor antagonist pegvisomant in patients with acromegaly resistant to long-term, high-dose somatostatin analog treatment: effect on IGF-I levels, tumor mass, hypertension and glucose tolerance  

Microsoft Academic Search

Objective: We aimed to investigate the efficacy of pegvisomant in patients with acromegaly resistant to long-term ( ^ 24-month), high-dose treatment with octreotide-LAR (40mg\\/month) or lanreotide (120mg\\/month). Design: This was an open, prospective study. Subjects and Methods: We studied 16 patients with acromegaly (nine women; aged 28-61 years). The main outcome measures were IGF-I levels, blood pressure, glucose tolerance and

Annamaria Colao; Rosario Pivonello; Renata S Auriemma; Maria Cristina De Martino; Martin Bidlingmaier; Francesco Briganti; Fabio Tortora; Pia Burman; Ione A Kourides; Christian J Strasburger; Gaetano Lombardi

2006-01-01

266

Orthostatic intolerance and tachycardia associated with norepinephrine-transporter deficiency  

NASA Technical Reports Server (NTRS)

BACKGROUND: Orthostatic intolerance is a syndrome characterized by lightheadedness, fatigue, altered mentation, and syncope and associated with postural tachycardia and plasma norepinephrine concentrations that are disproportionately high in relation to sympathetic outflow. We tested the hypothesis that impaired functioning of the norepinephrine transporter contributes to the pathophysiologic mechanism of orthostatic intolerance. METHODS: In a patient with orthostatic intolerance and her relatives, we measured postural blood pressure, heart rate, plasma catecholamines, and systemic norepinephrine spillover and clearance, and we sequenced the norepinephrine-transporter gene and evaluated its function. RESULTS: The patient had a high mean plasma norepinephrine concentration while standing, as compared with the mean (+/-SD) concentration in normal subjects (923 vs. 439+/-129 pg per milliliter [5.46 vs. 2.59+/-0.76 nmol per liter]), reduced systemic norepinephrine clearance (1.56 vs. 2.42+/-0.71 liters per minute), impairment in the increase in the plasma norepinephrine concentration after the administration of tyramine (12 vs. 56+/-63 pg per milliliter [0.07 vs. 0.33+/-0.37 pmol per liter]), and a disproportionate increase in the concentration of plasma norepinephrine relative to that of dihydroxyphenylglycol. Analysis of the norepinephrine-transporter gene revealed that the proband was heterozygous for a mutation in exon 9 (encoding a change from guanine to cytosine at position 237) that resulted in more than a 98 percent loss of function as compared with that of the wild-type gene. Impairment of synaptic norepinephrine clearance may result in a syndrome characterized by excessive sympathetic activation in response to physiologic stimuli. The mutant allele in the proband's family segregated with the postural heart rate and abnormal plasma catecholamine homeostasis. CONCLUSIONS: Genetic or acquired deficits in norepinephrine inactivation may underlie hyperadrenergic states that lead to orthostatic intolerance.

Shannon, J. R.; Flattem, N. L.; Jordan, J.; Jacob, G.; Black, B. K.; Biaggioni, I.; Blakely, R. D.; Robertson, D.

2000-01-01

267

Lactose intolerance. Pinpointing the source of nonspecific gastrointestinal symptoms.  

PubMed

Lactose intolerance is a common condition that can cause nonspecific gastrointestinal symptoms. A reliable diagnosis cannot be made on the basis of the patient's history. The breath hydrogen test is simple, noninvasive, accurate, and inexpensive and is the diagnostic method of choice. In addition to traditional dietary restriction of lactose, treatment may consist of alterations in dietary fat content or caloric density to reduce symptoms and use of dairy products or additives that provide lactase activity. PMID:2038590

Montes, R G; Perman, J A

1991-06-01

268

Genetic variation and lactose intolerance: detection methods and clinical implications.  

PubMed

The maturational decline in lactase activity renders most of the world's adult human population intolerant of excessive consumption of milk and other dairy products. In conditions of primary or secondary lactase deficiency, the lactose sugars in milk pass through the gastrointestinal tract undigested or are partially digested by enzymes produced by intestinal bacterial flora to yield short chain fatty acids, hydrogen, carbon dioxide, and methane. The undigested lactose molecules and products of bacterial digestion can result in symptoms of lactose intolerance, diarrhea, gas bloat, flatulence, and abdominal pain. Diagnosis of lactose intolerance is often made on clinical grounds and response to an empiric trail of dietary lactose avoidance. Biochemical methods for assessing lactose malabsorption in the form of the lactose breath hydrogen test and direct lactase enzyme activity performed on small intestinal tissue biopsy samples may also be utilized. In some adults, however, high levels of lactase activity persist into adulthood. This hereditary persistence of lactase is common primarily in people of northern European descent and is attributed to inheritance of an autosomal-dominant mutation that prevents the maturational decline in lactase expression. Recent reports have identified genetic polymorphisms that are closely associated with lactase persistence and nonpersistence phenotypes. The identification of genetic variants associated with lactase persistence or nonpersistence allows for molecular detection of the genetic predisposition towards adult-onset hypolactasia by DNA sequencing or restriction fragment length polymorphism analysis. The role for such genetic detection in clinical practice seems limited to ruling out adult-onset hypolactasia as a cause of intolerance symptoms but remains to be fully defined. Attention should be paid to appropriate interpretation of genetic detection in order to avoid potentially harmful reduction in dairy intake or misdiagnosis of secondary lactase deficiency. PMID:15287817

Sibley, Eric

2004-01-01

269

Metabolic Altera-ons in Pulmonary Arteries in Persistent Pulmonary Hypertension of the Newborn Bri;any Duffy, Annie Eis, Teresa Michalkiewicz, Ru-Jeng Teng, MD, Girija Ganesh Konduri, MD  

E-print Network

Metabolic Altera-ons in Pulmonary Arteries in Persistent Pulmonary Hypertension species in the pulmonary arteries in PPHN. Glucose-6-Phosphate Dehydrogenase (G and a;ain a hypertensive phenotype in pulmonary arteries, as seen in PPHN. We

270

Simultaneous renal hypertension and type 2 diabetes exacerbate vascular endothelial dysfunction in rats  

PubMed Central

Summary Despite the high rate of occurrence of both diabetes and hypertension in humans, the cardiovascular effects of the two conditions have not been investigated when they occur simultaneously. Thus this study examined the vascular effects of simultaneous type 2 diabetes and renal hypertension on endothelial function. Serum malondialdehyde and systolic blood pressure (SBP) were measured, glucose tolerance test (GTT) was performed, and concentration-response to phenylephrine (PE) in the absence and presence of nitro-l-arginine methyl ester (l-NAME), acetylcholine and sodium nitroprusside were conducted on aortic rings from diabetic control, type 2 diabetes, sham-operated, renal hypertensive, and simultaneous type 2 diabetes plus hypertension rats respectively. Hypertension, diabetes, and simultaneous diabetes and hypertension were associated with either increased or decreased maximal responses (Emax) of PE dependent on in the presence or absence of l-NAME. There was also increased serum malondialdehyde and decreased Emax of acetylcholine. Thus simultaneous hypertension and diabetes caused a greater decrease in Emax of acetylcholine compared to that seen with either diabetes or hypertension alone higher than that seen in hypertension. The blood glucose during GTT was lower than that seen in diabetes groups. Thus simultaneous type 2 diabetes and the SBP was renal hypertension is associated with improved glucose tolerance, but with further deterioration of endothelial dysfunction compared with either condition alone. PMID:22458508

Khalili, Azadeh; Nekooeian, Ali Akbar; Khosravi, Mohammad Bagher; Fakher, Shima

2012-01-01

271

Drug effects on orthostatic intolerance induced by bedrest  

NASA Technical Reports Server (NTRS)

Effective and practical preventive procedures for postflight orthostatic intolerance are highly desirable. The current practice of attempts to expand plasma volume by ingestion of salt and fluids before reentry has proven benefits. This study evaluated alternative options using fludrocortisone (F) to expand plasma volume (PV), dextroamphetamine (Dex) to enhance norepinephrine (NE) release, and atropine (A) to reduce the effects of vagal stimulation. Seven subjects with proven post-bedrest orthostatic intolerance returned for a 7-day 6-deg head-down bedrest study. F (0.2 mg) was given at 8:00 AM and 8:00 PM the day before and 8:00 AM the day the subjects got out of bed (2 hours before standing). PV was measured before and 1 hour after the last dose of F. Dex (5 mg) and A (0.8 mg) were then taken orally 1 hour before the stand test. F expanded PV by 16 percent and caused sodium retention. Four of the 7 subjects stood for 1 hour post-bedrest and heart rate, plasma NE and plasma renin responses to standing were greatly enhanced and sustained. Although there was a narrowing of pulse pressure, the ability to overcome orthostatic intolerance with these countermeasures was largely due to vasoconstriction and sustained high heart rate.

Vernikos, J.; Dallman, M. F.; Van Loon, G.; Keil, L. C.

1991-01-01

272

Creatinine clearance, pulse wave velocity, carotid compliance and essential hypertension  

Microsoft Academic Search

Creatinine clearance, pulse wave velocity, carotid compliance and essential hypertension.BackgroundThe vascular hallmark of subjects with end-stage renal disease is increased arterial stiffness independent of blood pressure, wall stress, and cardiovascular risk factors such as hypertension, plasma glucose and cholesterol, obesity, and tobacco consumption. Whether arterial stiffness and kidney function are statistically associated in subjects with plasma creatinine ?130 ?mol\\/L has

Jean-Jacques Mourad; Bruno Pannier; Jacques Blacher; Annie Rudnichi; Athanase Benetos; Gerard M. London; Michel E. Safar

2001-01-01

273

Skeletal Muscle Abnormalities in Pulmonary Arterial Hypertension  

PubMed Central

Background Pulmonary arterial hypertension is a progressive disease that is characterized by dyspnea and exercise intolerance. Impairment in skeletal muscle has recently been described in PAH, although the degree to which this impairment is solely determined by the hemodynamic profile remains uncertain. The aim of this study was to verify the association of structural and functional skeletal muscle characteristics with maximum exercise in PAH. Methods The exercise capacity, body composition, CT area of limb muscle, quality of life, quadriceps biopsy and hemodynamics of 16 PAH patients were compared with those of 10 controls. Results PAH patients had a significantly poorer quality of life, reduced percentage of lean body mass, reduced respiratory muscle strength, reduced resistance and strength of quadriceps and increased functional limitation at 6MWT and CPET. VO2 max was correlated with muscular variables and cardiac output. Bivariate linear regression models showed that the association between muscular structural and functional variables remained significant even after correcting for cardiac output. Conclusion Our study showed the coexistence of ventilatory and quadriceps weakness in face of exercise intolerance in the same group of PAH patients. More interestingly, it is the first time that the independent association between muscular pattern and maximum exercise capacity is evidenced in PAH, independently of cardiac index highlighting the importance of considering rehabilitation in the treatment strategy for PAH. PMID:25460348

Breda, Ana Paula; Pereira de Albuquerque, Andre Luis; Jardim, Carlos; Morinaga, Luciana Kato; Suesada, Milena Mako; Fernandes, Caio Julio Cesar; Dias, Bruno; Lourenço, Rafael Burgomeister; Salge, Joao Marcos; Souza, Rogerio

2014-01-01

274

Hepatic Carboxylesterase 1 Is Induced by Glucose and Regulates Postprandial Glucose Levels  

PubMed Central

Metabolic syndrome, characterized by obesity, hyperglycemia, dyslipidemia and hypertension, increases the risks for cardiovascular disease, diabetes and stroke. Carboxylesterase 1 (CES1) is an enzyme that hydrolyzes triglycerides and cholesterol esters, and is important for lipid metabolism. Our previous data show that over-expression of mouse hepatic CES1 lowers plasma glucose levels and improves insulin sensitivity in diabetic ob/ob mice. In the present study, we determined the physiological role of hepatic CES1 in glucose homeostasis. Hepatic CES1 expression was reduced by fasting but increased in diabetic mice. Treatment of mice with glucose induced hepatic CES1 expression. Consistent with the in vivo study, glucose stimulated CES1 promoter activity and increased acetylation of histone 3 and histone 4 in the CES1 chromatin. Knockdown of ATP-citrate lyase (ACL), an enzyme that regulates histone acetylation, abolished glucose-mediated histone acetylation in the CES1 chromatin and glucose-induced hepatic CES1 expression. Finally, knockdown of hepatic CES1 significantly increased postprandial blood glucose levels. In conclusion, the present study uncovers a novel glucose-CES1-glucose pathway which may play an important role in regulating postprandial blood glucose levels. PMID:25285996

Xu, Jiesi; Yin, Liya; Xu, Yang; Li, Yuanyuan; Zalzala, Munaf; Cheng, Gang; Zhang, Yanqiao

2014-01-01

275

Effect of indapamide SR in the treatment of hypertensive patients with type 2 diabetes  

Microsoft Academic Search

BackgroundTo evaluate the effect of the sustained-release formulation of indapamide (indapamide SR) in type 2 diabetic patients with mild-to-moderate hypertension and its possible side effects, particularly on glucose metabolism and lipid profiles.

Yi-Jen Hung; An-Tsz Hsieh; Ling-Yi Wu; Chang-Hsun Hsieh; Chih-Tsueng He; Tsao-Chin Yang; Wei-Cheng Lian; Shi-Wen Kuo

2003-01-01

276

Angiotensin II receptor blockers decreased blood glucose levels: a longitudinal survey using data from electronic medical records  

Microsoft Academic Search

BACKGROUND: A beneficial effect on glucose metabolism is reported with angiotensin receptor blocker (ARB) treatment of hypertension. The effect on blood glucose level during the course of treatment with ARBs in clinical cases is uncertain. Our objectives were to survey the changes in glucose and HbA1c levels in patients with hypertension over a one-year period, and to study the correlations

Noboru Kitamura; Yasuo Takahashi; Shuukoh Yamadate; Satoshi Asai

2007-01-01

277

Blood Glucose Monitoring Devices  

MedlinePLUS

... from an alternative sampling site to calibrate a continuous glucose monitor (CGM), or in insulin dosing calculations. ... How to Report Problems with Glucose Meters and Continuous Glucose Monitoring Systems Users of Blood Glucose Meters ...

278

Continuous Glucose Monitoring  

MedlinePLUS

... the upper arm, forearm, or thigh. What is continuous glucose monitoring? Continuous glucose monitoring (CGM) systems use a tiny sensor ... meter before making a change in treatment. 2 Continuous Glucose Monitoring CGM systems provide glucose measurements as ...

279

Determination of fructose metabolic pathways in normal and fructose-intolerant children: A sup 13 C NMR study using (U- sup 13 C)fructose  

SciTech Connect

An inborn deficiency in the ability of aldolase B to split fructose 1-phosphate is found in humans with hereditary fructose intolerance (HFI). A stable isotope procedure to elucidate the mechanism of conversion of fructose to glucose in normal children and in HFI children has been developed. A constant infusion of D-(U-{sup 13}C)fructose was given nasogastrically to control and to HFI children. Hepatic fructose conversion to glucose was estimated by examination of {sup 13}C NMR spectra of plasma glucose. Significantly lower values ({approx}3-fold) for fructose conversion to glucose were obtained for the HFI patients as compared to the controls. A quantitative determination of the metabolic pathways of fructose conversion to glucose was derived from {sup 13}C NMR measurement of plasma ({sup 13}C)glucose isotopomer populations. The finding of isotopomer populations of three adjacent {sup 13}C atoms at glucose C-4 ({sup 13}C{sub 3}-{sup 13}C{sub 4}-{sup 13}C{sub 5}) suggests that there is a direct pathway from fructose, by-passing fructose-1-phosphate aldolase, to fructose 1,6-bisphosphate. The metabolism of fructose by fructose-1-phosphate aldolase activity accounts for only {approx}50% of the total amount of hepatic fructose conversion to glucose. In view of the marked decline by 67% in synthesis of glucose from fructose in HFI subjects found in this study, the extent of ({sup 13}C)glucose formation from a trace amount of (U-{sup 13}C)fructose infused into the patient can be used as a safe and noninvasive diagnostic test for inherent faulty fructose metabolism.

Gopher, A.; Lapidot, A. (Weizmann Institute of Science, Rehovot (Israel)); Vaisman, N. (Kaplan Hospital, Rehovot (Israel)); Mandel, H. (Rambam Hospital, Haifa (Israel))

1990-07-01

280

Low renin hypertension  

PubMed Central

Low renin hypertension is an important and often underdiagnosed cause of hypertension. It may be associated with high aldosterone levels as in Conn's syndrome or low aldosterone levels as in Liddle syndrome, and syndrome of apparent mineralocorticoid excess, glucocorticoid remediable hypertension etc. Some forms of essential hypertension are also associated with low renin levels. Hypokalemia may be an important finding in low renin hypertension. The aldosterone to renin ratio helps in correct diagnosis. The treatment varies with etiology hence an accurate diagnosis is essential. Aldosterone antagonists play an important role in medical management of some varieties of low renin hypertension. PMID:23087856

Sahay, Manisha; Sahay, Rakesh K.

2012-01-01

281

Obesity?dependent dysregulation of glucose homeostasis in kinase suppressor of ras 2?/? mice  

PubMed Central

Abstract Disruption of KSR2 in humans and mice decreases metabolic rate and induces obesity, coincident with dysregulation of glucose homeostasis. Relative to wild?type mice, ksr2?/? mice are small prior to weaning with normal glucose tolerance at 6 weeks of age, but demonstrate excess adiposity by 9 weeks and glucose intolerance by 12–14 weeks. Defects in AICAR tolerance, a measure of whole?body AMPK activation, are detectable only when ksr2?/? mice are obese. Food restriction prevents the obesity of adult ksr2?/? mice and normalizes glucose and AICAR sensitivity. Obesity and glucose intolerance return when ad lib feeding is restored to the diet?restricted mice, indicating that glucose dysregulation is secondary to obesity in ksr2?/? mice. The phenotype of C57BL/6 ksr2?/? mice, including obesity and obesity?related dysregulation of glucose homeostasis, recapitulates that of humans with KSR2 mutations, demonstrating the applicability of the C57BL/6 ksr2?/? mouse model to the study of the pathogenesis of human disease. These data implicate KSR2 as a physiological regulator of glucose metabolism during development affecting energy sensing, insulin signaling, and lipid storage, and demonstrate the value of the C57BL/6 ksr2?/? mouse model as a unique and relevant model system in which to develop and test therapeutic targets for the prevention and treatment of obesity, type 2 diabetes, and obesity?related metabolic disorders. PMID:24997067

Henry, MaLinda D.; Costanzo?Garvey, Diane L.; Klutho, Paula J.; Lewis, Robert E.

2014-01-01

282

Hemodynamic and Biochemical Changes after Chronic Administration of Cilazapril to Hypertensive Patients  

Microsoft Academic Search

The study describes the changes in basic hemodynamic parameters after long-term antihypertensive therapy with cilazapril - a new ACE inhibitor lacking a sulfhydryl group - in hypertensive patients and the drug effects on renal function, glucose tolerance and lipid metabolism. 30 patients (18 males, 12 females, mean age: 53.3 ± 18 years) with mild to moderate essential hypertension were studied.

N. Lejkos; A. Efthimiadis; I. Liatsis; G. Boudonas; A. Papachristou; D. Platoyannis

1993-01-01

283

Neuronal LRP1 Regulates Glucose Metabolism and Insulin Signaling in the Brain.  

PubMed

Alzheimer's disease (AD) is a neurological disorder characterized by profound memory loss and progressive dementia. Accumulating evidence suggests that Type 2 diabetes mellitus, a metabolic disorder characterized by insulin resistance and glucose intolerance, significantly increases the risk for developing AD. Whereas amyloid-? (A?) deposition and neurofibrillary tangles are major histological hallmarks of AD, impairment of cerebral glucose metabolism precedes these pathological changes during the early stage of AD and likely triggers or exacerbates AD pathology. However, the mechanisms linking disturbed insulin signaling/glucose metabolism and AD pathogenesis remain unclear. The low-density lipoprotein receptor-related protein 1 (LRP1), a major apolipoprotein E receptor, plays critical roles in lipoprotein metabolism, synaptic maintenance, and clearance of A? in the brain. Here, we demonstrate that LRP1 interacts with the insulin receptor ? in the brain and regulates insulin signaling and glucose uptake. LRP1 deficiency in neurons leads to impaired insulin signaling as well as reduced levels of glucose transporters GLUT3 and GLUT4. Consequently, glucose uptake is reduced. By using an in vivo microdialysis technique sampling brain glucose concentration in freely moving mice, we further show that LRP1 deficiency in conditional knock-out mice resulted in glucose intolerance in the brain. We also found that hyperglycemia suppresses LRP1 expression, which further exacerbates insulin resistance, glucose intolerance, and AD pathology. As loss of LRP1 expression is seen in AD brains, our study provides novel insights into insulin resistance in AD. Our work also establishes new targets that can be explored for AD prevention or therapy. PMID:25855193

Liu, Chia-Chen; Hu, Jin; Tsai, Chih-Wei; Yue, Mei; Melrose, Heather L; Kanekiyo, Takahisa; Bu, Guojun

2015-04-01

284

Increased methylglyoxal and advanced glycation end products in kidney from spontaneously hypertensive rats  

Microsoft Academic Search

Increased methylglyoxal and advanced glycation end products in kidney from spontaneously hypertensive rats.BackgroundMethylglyoxal (MG), a metabolite of glucose, causes nonenzymatic glycation of proteins to form irreversible advanced glycation end products (AGEs). The role of MG in the development of essential hypertension is unknown, although MG has been extensively studied in relation to diabetes.MethodsBlood pressure of spontaneously hypertensive rats (SHR) and

XIAOXIA WANG; KAUSHIK DESAI; JES THORN CLAUSEN; LINGYUN WU

2004-01-01

285

What Is Pulmonary Hypertension?  

MedlinePLUS

... Dizziness Shortness of breath Symptoms and diagnosis of primary pulmonary hypertension (PPH) can be tricky. Early on, you may ... a definite health problem that needs treatment. Although primary pulmonary hypertension (PPH) is rare, diagnosing and treating PPH is ...

286

Drug-induced hypertension  

MedlinePLUS

... induced hypertension are the same as those of primary hypertension, and may include: Anxiety Chest pain Confusion Excessive perspiration Headache Muscle tremors Nausea and vomiting Pale skin or redness Tiredness ...

287

Cardiovascular hypertensive emergencies.  

PubMed

Inevitably, a small proportion of patients with systematic hypertension will develop hypertensive crisis at some point. Hypertensive crises can be divided into hypertensive emergency or hypertensive urgency according to the presence or lack of acute target organ damage. In this review, we discuss cardiovascular hypertensive emergencies, including acute coronary syndrome, aortic dissection, congestive heart failure, and sympathomimetic hypertensive crises, including those caused by cocaine use. Each presents in a unique fashion, although some hypertensive emergency patients report nonspecific symptoms. Treatment includes several effective and rapid-acting medications to safely reduce the blood pressure, protect remaining end-organ function, relieve symptoms, minimize the risk of complications, and thereby improve patient outcomes. PMID:25620633

Papadopoulos, D P; Sanidas, E A; Viniou, N A; Gennimata, V; Chantziara, V; Barbetseas, I; Makris, T K

2015-02-01

288

Relationship of Glucose and Insulin Levels to the Risk of Myocardial Infarction: A Case-Control Study  

Microsoft Academic Search

BACKGROUND Nondiabetic hyperglycemia may be an important cardiac risk factor. The relationship between myocardial infarction and glucose, insulin, abdominal obesity, lipids and hypertension was therefore studied in South Asians—a group at high risk for coronary heart disease and diabetes. METHODS Demographics, waist\\/hip ratio, fasting blood glucose (FBG), insulin, lipids and glucose tolerance were measured in 300 consecutive patients with a

Hertzel C. Gerstein; Prem Pais; Janice Pogue; Salim Yusuf

289

PPAR? regulates glucose metabolism and insulin sensitivity  

PubMed Central

The metabolic syndrome is a collection of obesity-related disorders. The peroxisome proliferator-activated receptors (PPARs) regulate transcription in response to fatty acids and, as such, are potential therapeutic targets for these diseases. We show that PPAR? (NR1C2) knockout mice are metabolically less active and glucose-intolerant, whereas receptor activation in db/db mice improves insulin sensitivity. Euglycemic–hyperinsulinemic-clamp experiments further demonstrate that a PPAR?-specific agonist suppresses hepatic glucose output, increases glucose disposal, and inhibits free fatty acid release from adipocytes. Unexpectedly, gene array and functional analyses suggest that PPAR? ameliorates hyperglycemia by increasing glucose flux through the pentose phosphate pathway and enhancing fatty acid synthesis. Coupling increased hepatic carbohydrate catabolism with its ability to promote ?-oxidation in muscle allows PPAR? to regulate metabolic homeostasis and enhance insulin action by complementary effects in distinct tissues. The combined hepatic and peripheral actions of PPAR? suggest new therapeutic approaches to treat type II diabetes. PMID:16492734

Lee, Chih-Hao; Olson, Peter; Hevener, Andrea; Mehl, Isaac; Chong, Ling-Wa; Olefsky, Jerrold M.; Gonzalez, Frank J.; Ham, Jungyeob; Kang, Heonjoong; Peters, Jeffrey M.; Evans, Ronald M.

2006-01-01

290

Secondary Forms of Hypertension  

Microsoft Academic Search

\\u000a In most studies, hypertension in children has been secondary to an identifiable cause in a large majority of those studied\\u000a (1,2). This has changed during the relatively recent epidemic of childhood obesity, where primary hypertension in many centers\\u000a now is the most common cause form of hypertension (3). In adults primary hypertension is the dominating diagnosis. This chapter will discuss

Kjell Tullus

291

Autogenic-feedback training: A countermeasure for orthostatic intolerance  

NASA Technical Reports Server (NTRS)

NASA has identified cardiovascular deconditioning as a serious biomedical problem associated with long-duration exposure to microgravity in space. High priority has been given to the development of countermeasures for this disorder and the resulting orthostatic intolerance experienced by crewmembers upon their return to the 1g norm of Earth. The present study was designed to examine the feasibility of training human subjects to control their own cardiovascular responses to gravitational stimulation (i.e., a tilt table). Using an operant conditioning procedure, Autogenic-Feedback Training (AFT), we would determine if subjects could learn to increase their own blood pressure voluntarily.

Cowings, Patricia S.; Toscano, William B.; Kamiya, Joe; Miller, Neal E.; Pickering, Thomas G.

1991-01-01

292

Hypertension in developing countries.  

PubMed

The past 2 decades have seen a considerable global increase in cardiovascular disease, with hypertension remaining by far the most common. More than one-third of adults in Africa are hypertensive; as in the urban populations of most developing countries. Being a condition that occurs with relatively few symptoms, hypertension remains underdetected in many countries; especially in developing countries where routine screening at any point of health care is grossly underutilized. Because hypertension is directly related to cardiovascular disease, this has led to hypertension being the leading cause of adverse cardiovascular outcomes, as a result of patients living, often unknowingly, with uncontrolled hypertension for prolonged periods of time. In Africa, hypertension is the leading cause of heart failure; whereas at global levels, hypertension is responsible for more than half of deaths from stroke, just less than half of deaths from coronary artery disease, and for more than one-tenth of all global deaths. In this review, we discuss the escalating occurrence of hypertension in developing countries, before exploring the strengths and weaknesses of different measures to control hypertension, and the challenges of adopting these measures in developing countries. On a broad level, these include steps to curb the ripple effect of urbanization on the health and disease profile of developing societies, and suggestions to improve loopholes in various aspects of health care delivery that affect surveillance and management of hypertension. Furthermore, we consider how the industrial sectors' contributions toward the burden of hypertension can also be the source of the solution. PMID:24786443

Tibazarwa, Kemi B; Damasceno, Albertino A

2014-05-01

293

Primary Prevention of Hypertension  

E-print Network

Primary Prevention of Hypertension: Clinical and Public Health Advisory from the National High NIH PUBLICATION NO. 02-5076 NOVEMBER 2002 Primary Prevention of Hypertension: Clinical and Public LIFETIME BURDEN OF ELEVATED BLOOD PRESSURE 3 APPROACHES TO PRIMARY PREVENTION OF HYPERTENSION 4 Population

Bandettini, Peter A.

294

Treadmill Aerobic Training Improves Glucose Tolerance and Indices of Insulin Sensitivity in Disabled Stroke Survivors A Preliminary Report  

Microsoft Academic Search

Background and Purpose—Insulin resistance and glucose intolerance are highly prevalent after stroke, contributing to worsening cardiovascular disease risk and a predisposition to recurrent stroke. Treadmill exercise training (T-AEX) increases aerobic capacity (VO2 peak) in chronic stroke patients, suggesting intensity levels that may be adequate to improve glucose metabolism. We compared the effects of a progressive T-AEX intervention to an attention-matched

Frederick M. Ivey; Alice S. Ryan; Charlene E. Hafer-Macko; Andrew P. Goldberg; Richard F. Macko

295

Efficacy of Garcinia Cambogia on Body Weight, Inflammation and Glucose Tolerance in High Fat Fed Male Wistar Rats  

PubMed Central

Introduction: Obesity leads to derangements in lipid and glucose homeostasis resulting in various metabolic complications. Plants containing vital phytochemicals are known to posses anti obesity properties and have proved to exert beneficial effects in obesity. Objectives: The present study was aimed to investigate the effects of Garcinia Cambogia on body weight, glucose tolerance and inflammation in high fat diet fed male Wistar rats. Materials and Methods: Five month old male wistar rats (n=40) were divided into four groups. Two groups were fed with standard rodent diet and the remaining two with 30% high fat diet. One group in each of the two sets received the crude ethanolic extract of Garcinia Cambogia at a dose of 400mg/kg body weight/day for ten weeks. Body weight, intraperitoneal glucose tolerance test, leptin, tumour necrosis factor-? (TNF-?) and renal function (urea, creatinine, uric acid) were studied. Results: High fat diet fed rats showed increased body weight gain, glucose intolerance, elevated levels of plasma leptin and TNF-?. Supplementation of Garcinia Cambogia extract (GE) along with high fat diet significantly decreased body weight gain, glucose intolerance, plasma leptin and TNF-? level. No significant changes were observed in the renal function parameters in any of the groups. Conclusion: Supplementation of the Garcinia Cambogia extract with high fat diet reduced body weight gain, inflammation and glucose intolerance.

Sripradha, Ramalingam

2015-01-01

296

Differentiating intolerance of uncertainty from three related but distinct constructs.  

PubMed

Individual differences in uncertainty have been associated with heightened anxiety, stress and approach-oriented coping. Intolerance of uncertainty (IU) is a trait characteristic that arises from negative beliefs about uncertainty and its consequences. Researchers have established the central role of IU in the development of problematic worry and maladaptive coping, highlighting the importance of this construct to anxiety disorders. However, there is a need to improve our understanding of the phenomenology of IU. The goal of this paper was to present hypotheses regarding the similarities and differences between IU and three related constructs--intolerance of ambiguity, uncertainty orientation, and need for cognitive closure--and to call for future empirical studies to substantiate these hypotheses. To assist with achieving this goal, we conducted a systematic review of the literature, which also served to identify current gaps in knowledge. This paper differentiates these constructs by outlining each definition and general approaches to assessment, reviewing the existing empirical relations, and proposing theoretical similarities and distinctions. Findings may assist researchers in selecting the appropriate construct to address their research questions. Future research directions for the application of these constructs, particularly within the field of clinical and health psychology, are discussed. PMID:23849047

Rosen, Natalie O; Ivanova, Elena; Knäuper, Bärbel

2014-01-01

297

Protecting renal function in the hypertensive patient: Clinical guidelines  

Microsoft Academic Search

Both the incidence and prevalence of chronic kidney disease (CKD) are increasing in the United States and worldwide. Patients with both diabetes and hypertension have a dramatically increased risk of cardiovascular and renal events, particularly if both conditions are not effectively controlled. Failure to achieve the goals for blood glucose, blood pressure (BP), and lipids is associated with high morbidity

George L. Bakris

2005-01-01

298

Recovery of oral glucose tolerance by Wistar rats after treatment with Coreopsis tinctoria infusion.  

PubMed

Infusions of Coreopsis tinctoria flowering tops have traditionally been used in Portugal to control hyperglycaemia but no pharmacological or toxicological studies have been reported until now. The chalcones marein and okanin were isolated from the aqueous extract, together with the 2S-3',4',7,8-tetrahydroxyflavanone. The content of marein in extracts was determined by HPLC-UV and the radical scavenging capacity evaluated by the DPPH method (EC(50) = 21 microg/mL). Glucose intolerance was induced by a single intraperitoneal injection of streptozotocin in saline (40 mg/Kg). After three weeks of oral treatment with C. tinctoria extract (500 mg/Kg/day) the animals were no longer glucose-intolerant (p > 0.05). Additionally, this oral treatment caused no hepatotoxicity in the rats, as determined by blood alanine and aspartate transaminases. A single administration of extract had no effect on oral glucose tolerance in normal Wistar rats. The extract also had no effect on insulin secretion by MIN6 cells. In conclusion, C. tinctoria infusion is able to abolish the streptozotocin-induced glucose-intolerance in rats after three weeks of oral treatment by a mechanism other than induction of insulin secretion. The recovery of beta-pancreatic function mediated by an antioxidant mechanism is a possibility that deserves further investigation. PMID:19827015

Dias, Teresa; Mota-Filipe, Hélder; Liu, Bo; Jones, Peter; Houghton, Peter J; Paulo, Alexandra

2010-05-01

299

A comparison of intolerance of uncertainty in analogue obsessive-compulsive disorder and generalized anxiety disorder  

Microsoft Academic Search

Intolerance of uncertainty has been defined as the unwillingness to tolerate the possibility that negative events may occur in the future, no matter how low the probability [Personality Individual Differences 17 (1994), 791–802]. Previous research suggests that intolerance of uncertainty may be more specific to worry and generalized anxiety disorder (GAD) than to other anxiety disorders [e.g., Dugas, M. J.,

Robert M. Holaway; Richard G. Heimberg; Meredith E. Coles

2006-01-01

300

Studies on Intolerance in American Life. Program in American History and Civilization.  

ERIC Educational Resources Information Center

The narrative selected for this unit on intolerance illustrates the perennial and universal methods for scapegoating. The general teaching objectives are to lead the students: 1) to feelings of tolerance toward individuals and groups who are different; 2) to investigate intolerance in terms of some of its causes: fear, deprivation, threatened…

Tufts Univ., Medford, MA. Lincoln Filene Center for Citizenship and Public Affairs.

301

Prevalence of self-reported lactose intolerance in multiethnic sample of adults  

Technology Transfer Automated Retrieval System (TEKTRAN)

According to the National Institute of Diabetes and Digestive and Kidney Diseases, between 30 and 50 million Americans have the potential for lactose-intolerance symptoms. However, lactose-intolerance prevalence rates in practical life settings may be lower than originally suggested. The goal of thi...

302

Lactose Intolerance: Exploring Reaction Kinetics Governing Lactose Conversion of Dairy Products within the Undergraduate Laboratory  

ERIC Educational Resources Information Center

Lactose intolerance is a condition suffered by an estimated 50 million Americans. Certain ethnic and racial populations are more widely affected than others. As many as 75 percent of all African-American, Jewish, Native American, and Mexican-American adults, and 90 percent of Asian-American adults are lactose intolerant. Some populations in Africa…

Smart, Jimmy L.

2008-01-01

303

Orthostatic intolerance and the postural tachycardia syndrome: genetic and environment pathophysiologies  

Microsoft Academic Search

Orthostatic intolerance is a common problem for inbound space travelers. There is usually tachycardia on standing but blood pressure may be normal, low or, rarely, elevated. This condition is analogous to the orthostatic intolerance that occurs on Earth in individuals with orthostatic tachycardia, palpitations, mitral valve prolapse, and light-headedness. Our studies during the Neurolab mission indicated that sympathetic nerve traffic

David Robertson; John R. Shannon; Italo Biaggioni; Andrew C. Ertl; André Diedrich; Robert Carson; Raffaello Furlan; Giris Jacob; Jens Jordan

2000-01-01

304

HRQoL questionnaire evaluation in lactose intolerant patients with adverse reactions to foods.  

PubMed

The occurrence of patients with gastrointestinal symptoms attributed either to food allergy or intolerance has significantly increased. Nevertheless, an accurate and detailed case history, a systematic evaluation and the outcomes of specific allergy tests to identify the offending foods, including "in vivo" and "in vitro" allergy tests, are often negative for food allergy and may indicate a lactose intolerance, which is a recurrent condition affecting about 50% of adults. The aims of our study were the following: (1) What is the real incidence of the food hypersensitivity and the primary lactose intolerance in patients with gastrointestinal symptoms, initially referred to allergy or food intolerance? (2) Does lactose intolerance affect the quality of life and compliance to the therapy program? We investigated 262 consecutive patients, 72 men and 190 women. An accurate and detailed history and clinical examination were completed to investigate the offending foods. The evaluation in each patient included: allergy tests, lactose H2 breath test (LHBT) and the HRQoL questionnaire. Five years after the diagnosis of lactose intolerance, a questionnaire on the persistence of gastrointestinal symptoms after lactose ingestion and the diet compliance was distributed. Our results demonstrate an high prevalence of lactose intolerance, more frequent in women; in these patients, bloating and diarrhea are the most reported symptoms. We observe only a significant positive correlation between adverse drug reaction (ADR) and LHBT+ patients, but not an augmented prevalence of food allergy and a negative impact on the HRQoL questionnaire of lactose intolerance. PMID:21614464

Erminia, Ridolo; Ilaria, Baiardini; Tiziana, Meschi; Silvia, Peveri; Antonio, Nouvenne; Pierpaolo, Dall'Aglio; Loris, Borghi

2013-09-01

305

Blood Glucose Log  

MedlinePLUS

... cut here ¢ cut here ¢ If you have high blood glucose , make notes in your log and talk with ... plan, physical activity, or diabetes medicines. Having low blood glucose means that your blood glucose level is too ...

306

Blood Test: Glucose  

MedlinePLUS

... Sports: Keeping Kids Safe Concussions: What to Know Blood Test: Glucose KidsHealth > Parents > Doctors & Hospitals > Medical Tests & Exams > Blood ... If You Have Questions What It Is A blood glucose test measures the amount of glucose (the main ...

307

Prevalence of diabetes in Catalonia (Spain): an oral glucose tolerance test-based population study  

Microsoft Academic Search

The goal of this study was to investigate the prevalence of diabetes mellitus and impaired glucose tolerance in the adult population of Catalonia and study their association with obesity, central obesity, hypertension and smoking habit. A random sample of 3839 subjects aged 30–89 years participated in this cross-sectional study: 2214 subjects underwent a health examination with oral glucose tolerance test

Conxa Castell; Ricard Tresserras; Jaume Serra; Albert Goday; Gonçal Lloveras; Llu??s Salleras

1999-01-01

308

Oxidative stress — mediated alterations in glucose dynamics in a genetic animal model of type II diabetes  

Microsoft Academic Search

Insulin resistance, characterized by an inexorable decline in skeletal muscle glucose utilization and\\/or an excessive hepatic glucose production, constitutes a major pathogenic importance in a cluster of clinical disorders including diabetes mellitus, hypertension, dyslipidemia, central obesity and coronary artery disease. A novel concept suggests that heightened state of oxidative stress during diabetes contributes, at least in part, to the development

Milad S. Bitar; Eyad AL-Saleh; Fahd AL-Mulla

2005-01-01

309

[Endocrine disorders associated with impaired glucose tolerance].  

PubMed

Endocrine disorders associated with diabetes mellitus are described. When blood glucose control deteriorates, observed endocrine abnormalities are as follows. 1) Blood GH levels increase. This elevation is small but enough to disturb insulin secretion and glucose metabolism. Plama insulin-like growth factor-1 levels decrease in spite of their strong relation with diabetic retinopathy. 2) Blood thyroid hormones show the similarity with low T3 syndrome. 3) Hyporeninemic hypoaldosteronism occurs especially with patients who have hypertension or moderate diabetic complications. 4) Plasma pancreatic glucagon levels are elevated. Amino acids induce hypersecretion but hypoglycemia fails to response normally. Glucose administration shows impaired inhibition or paradoxical hypersecretion. 5) Other plasma levels of pancreatic hormones such as gastrin, secretin, motilin and somatostatin are usually elevated. PMID:8914425

Ogino, Y; Toriumi, M; Tanaka, K

1996-10-01

310

Riociguat for pulmonary hypertension.  

PubMed

Pulmonary hypertension, an elevation of the mean pulmonary artery pressure ?25 mmHg, ultimately leads to premature death due to right ventricular dysfunction. Ten treatments from three classes of drugs are licensed for the management of pulmonary arterial hypertension. These treatments have improved exercise capacity but median survival is still poor. Additionally there are no licensed therapies for the other groups of pulmonary hypertension. Riociguat is a novel drug that stimulates soluble guanylate cyclase independently of nitric oxide and in synergy with nitric oxide. This review summarises the available evidence for riociguat in the treatment across all groups of pulmonary hypertension with a focus on pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension. PMID:24580082

Cannon, John E; Pepke-Zaba, Joanna

2014-05-01

311

The baroreflex in hypertension.  

PubMed

Hypertension is a complex syndrome that increases the risk of developing other medical comorbidities and interacts with other medical conditions to increase the risk of target end-organ damage such as cardiovascular disease, stroke, and renal disease. Hypertension remains under-recognized and poorly controlled in the USA and worldwide. In some patients, hypertension is resistant to optimal medical therapy. Over the last few decades, there has been an increasing understanding of the role of the sympathetic nervous system in the development and maintenance of hypertension. This update reviews the physiology and role of the sympathetic nervous system in hypertension and pharmacological and interventional treatments directed at nervous system involvement in secondary hypertension. PMID:25754323

Fernandez, Genaro; Lee, Junsoo Alex; Liu, Lynn C; Gassler, John P

2015-04-01

312

Nurse management for hypertension  

Microsoft Academic Search

Background: Standard office-based approaches to controlling hypertension show limited success. Such suboptimal hypertension control reflects in part the absence of both an infrastructure for patient education and frequent, regular blood pressure (BP) monitoring. We tested the efficacy of a physician-directed, nurse-managed, home-based system for hypertension management with standardized algorithms to modulate drug therapy, based on patients’ reports of home BP.Methods:

Peter Rudd; Nancy Houston Miller; Judy Kaufman; Helena C. Kraemer; Albert Bandura; George Greenwald; Robert F. Debusk

2004-01-01

313

Pulmonary Hypertension after Splenectomy?  

Microsoft Academic Search

Results: The prevalence of asplenia in patients with pul- monary hypertension was 11.5% (95% CI, 4.7% to 22.2%) compared with 0% (CI, 0% to 3.2%) in those without pulmonary hypertension (P , 0.001). Histopathologic ex- amination of lung specimens from patients with postsple- nectomy pulmonary hypertension showed intimal fibrosis, plexiform lesions, and abundant thrombotic lesions. Conclusion: Patients who have had

Marius M. Hoeper; Jost Niedermeyer; Frank Hoffmeyer; Peer Flemming; Helmut Fabel

314

Pathogenesis of Hypertension  

NSDL National Science Digital Library

Physiology in Medicine review article A clearer understanding of the pathogenesis of hypertension will probably lead to more highly targeted therapies and to greater reduction in hypertension-related cardiovascular disease morbidity than can be achieved with current empirical treatment. Hypertension clusters in families and results from a complex interaction of genetic and environmental factors. Endothelial dysfunction, increased vascular reactivity, and vascular remodeling may be causes, rather than consequences, of blood pressure elevation; increased vascular stiffness contributes to isolated systolic hypertension in the elderly.

MD Suzanne Oparil (University of Alabama at Birmingham Department of Medicine)

2003-11-04

315

Impaired glucose tolerance in rats fed low-carbohydrate, high-fat diets.  

PubMed

Moderate low-carbohydrate/high-fat (LC-HF) diets are widely used to induce weight loss in overweight subjects, whereas extreme ketogenic LC-HF diets are used to treat neurological disorders like pediatric epilepsy. Usage of LC-HF diets for improvement of glucose metabolism is highly controversial; some studies suggest that LC-HF diets ameliorate glucose tolerance, whereas other investigations could not identify positive effects of these diets or reported impaired insulin sensitivity. Here, we investigate the effects of LC-HF diets on glucose and insulin metabolism in a well-characterized animal model. Male rats were fed isoenergetic or hypocaloric amounts of standard control diet, a high-protein "Atkins-style" LC-HF diet, or a low-protein, ketogenic, LC-HF diet. Both LC-HF diets induced lower fasting glucose and insulin levels associated with lower pancreatic ?-cell volumes. However, dynamic challenge tests (oral and intraperitoneal glucose tolerance tests, insulin-tolerance tests, and hyperinsulinemic euglycemic clamps) revealed that LC-HF pair-fed rats exhibited impaired glucose tolerance and impaired hepatic and peripheral tissue insulin sensitivity, the latter potentially being mediated by elevated intramyocellular lipids. Adjusting visceral fat mass in LC-HF groups to that of controls by reducing the intake of LC-HF diets to 80% of the pair-fed groups did not prevent glucose intolerance. Taken together, these data show that lack of dietary carbohydrates leads to glucose intolerance and insulin resistance in rats despite causing a reduction in fasting glucose and insulin concentrations. Our results argue against a beneficial effect of LC-HF diets on glucose and insulin metabolism, at least under physiological conditions. Therefore, use of LC-HF diets for weight loss or other therapeutic purposes should be balanced against potentially harmful metabolic side effects. PMID:23982154

Bielohuby, Maximilian; Sisley, Stephanie; Sandoval, Darleen; Herbach, Nadja; Zengin, Ayse; Fischereder, Michael; Menhofer, Dominik; Stoehr, Barbara J M; Stemmer, Kerstin; Wanke, Rüdiger; Tschöp, Matthias H; Seeley, Randy J; Bidlingmaier, Martin

2013-11-01

316

Strict dietary sodium reduction worsens insulin sensitivity by increasing sympathetic nervous activity in patients with primary hypertension  

Microsoft Academic Search

To assess the effects of sodium reduction on insulin sensitivity in hypertension, we examined the change of insulin sensitivity after two degrees of dietary sodium restriction by the euglycemic hyperinsulinemic glucose clamp method in 12 subjects with primary hypertension. A controlled period of 1 week, when the subjects were taking a normal sodium diet, was followed by a randomized crossover

Tomoko Gomi; Yuko Shibuya; Jun Sakurai; Nobuhito Hirawa; Kyoko Hasegawa; Toshio Ikeda

1998-01-01

317

Predictors of Hypertension Among Filipino Immigrants in the Northeast US  

PubMed Central

Hypertension remains disproportionately high among Filipinos compared to other racial and ethnic minority populations, and little research on cardiovascular disease risk factors has been conducted among Filipino immigrants in the Northeastern part of the United States. To determine hypertension prevalence and risk factors among Filipino Americans in the New York City area, blood pressure and other clinical measurements were taken from a sample of Filipino Americans during 119 community health screenings conducted between 2006 and 2010. Additional socio-demographic and health-related characteristics were also collected via a cross-sectional survey. A total of 1,028 Filipino immigrants completed the survey and had clinical readings collected. Bivariate analyses and logistic regression were performed in order to predict and assess risk factors for hypertension among our sample. Fifty-three percent of individuals were hypertensive, and half of hypertensive individuals were uninsured. Logistic regression indicated that older age, male gender, living in the United States for over 5 years, a BMI greater than 23.0 kg/m2, an elevated glucose reading, a family history of hypertension, and fair or poor self-reported health status were predictors of hypertension. There is a great need to develop more effective community-based interventions in the Filipino community to address cardiovascular health disparities. PMID:23553685

Islam, Nadia Shilpi; Aguilar, David E.; Wyatt, Laura C.; Tandon, S. Darius; Abesamis-Mendoza, Noilyn; Nur, Potri Ranka Manis Queano; Rago-Adia, Josephine; Ileto, Benjamin; Rey, Mariano J.; Trinh-Shevrin, Chau

2013-01-01

318

Lactose intolerance and African Americans: implications for the consumption of appropriate intake levels of key nutrients.  

PubMed

Lactose intolerance is a complex condition that is complicated by cultural beliefs and perceptions about the consumption of dairy products. These attitudes about dairy may contribute to inadequate intake of key nutrients that may impact conditions that contribute to health disparities in African Americans. While a complex health problem, lactose intolerance is easy to treat. However, no treatment can improve the body's ability to produce lactase. Yet, symptoms can be controlled through dietary strategies. This position paper emphasizes the importance of using patient and provider-level strategies in order to reduce the risks to the health of African Americans that may accrue as a result of dairy nutrient deficiency. Evaluation and assessment of interventions tested is critical so that evidence-based approaches to addressing dairy nutrient deficiency and lactose Intolerance can be created. Lastly, it is essential for physicians to communicate key messages to their patients. Since dairy nutrients address important health concerns, the amelioration of lactose intolerance is an investment in health. Lactose intolerance is common, is easy to treat, and can be managed. It is possible to consume dairy even in the face of a history of maldigestion or lactose intolerant issues. Gradually increasing lactose in the diet--drinking small milk portions with food, eating yogurt, and consuming cheese--are effective strategies for managing lactose intolerance and meeting optimal dairy needs. PMID:19899495

2009-10-01

319

Four faces of baroreflex failure: hypertensive crisis, volatile hypertension, orthostatic tachycardia, and malignant vagotonia  

NASA Technical Reports Server (NTRS)

BACKGROUND: The baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences. METHODS AND RESULTS: Impairment of the baroreflex may produce an unusually broad spectrum of clinical presentations; with acute baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-term follow-up. With incomplete loss of baroreflex afferents, a mild syndrome of orthostatic tachycardia or orthostatic intolerance may appear. Finally, if the baroreflex failure occurs without concomitant destruction of the parasympathetic efferent vagal fibers, a resting state may lead to malignant vagotonia with severe bradycardia and hypotension and episodes of sinus arrest. CONCLUSIONS: Although baroreflex failure is not the most common cause of the above conditions, correct differentiation from other cardiovascular disorders is important, because therapy of baroreflex failure requires specific strategies, which may lead to successful control.

Ketch, Terry; Biaggioni, Italo; Robertson, RoseMarie; Robertson, David

2002-01-01

320

The acceptability of milk and milk products in populations with a high prevalence of lactose intolerance.  

PubMed

1) Most humans, like other mammals, gradually lose the intestinal enzyme lactase after infancy and with it the ability to digest lactose, the principle sugar in milk. At some point in prehistory, a genetic mutation occurred and lactase activity persisted in a majority of the adult population of Northern and Central Europe. 2) Persistence of intestinal lactase, the uncommon trait worldwide, is inherited as a highly penetrant autosomal-dominant characteristic. Both types of progeny are almost equally common when one parent is a lactose maldigester and the other a lactose digester. 3) The incidence of lactose maldigestion is usually determined in adults by the administration in the fasting state of a 50-g dose of lactose in water, the equivalent of that in 1 L of milk. Measurement is made of either the subsequent rise in blood glucose or the appearance of additional hydrogen in the breath. It is also sometimes identified by measuring lactase activity directly in a biopsy sample from the jejunum. For children the test dose is reduced according to weight. Depending on the severity of the lactase deficiency and other factors, the test dose may result in abdominal distention, pain, and diarrhea. 4) The frequency of lactose maldigestion varies widely among populations but is high in nearly all but those of European origin. In North American adults lactose maldigestion is found in approximately 79% of Native Americans, 75% of blacks, 51% of Hispanics, and 21% of Caucasians. In Africa, Asia, and Latin America prevalence rates range from 15-100% depending on the population studied. 5) Whenever the lactose ingested exceeds the capacity of the intestinal lactase to split it into the simple sugars glucose and galactose, which are absorbed directly, it passes undigested to the large intestine. There it is fermented by the colonic flora, with short-chain fatty acids and hydrogen gas as major products. The gas produced can cause abdominal distention and pain and diarrhea may also result from the fermentation products. 6) Among individuals with incomplete lactose digestion, there is considerable variation in awareness of lactose intolerance and in the quantity of lactose that can be ingested without symptoms. A positive standard lactose test is not a reliable predictor of the ability of an individual to consume moderate amounts of milk and milk products without symptoms. In usual situations the quantity of lactose ingested at any one time is much less than in the lactose-tolerance test.(ABSTRACT TRUNCATED AT 400 WORDS) PMID:3140651

Scrimshaw, N S; Murray, E B

1988-10-01

321

FGF19 action in the brain induces insulin-independent glucose lowering  

PubMed Central

Insulin-independent glucose disposal (referred to as glucose effectiveness [GE]) is crucial for glucose homeostasis and, until recently, was thought to be invariable. However, GE is reduced in type 2 diabetes and markedly decreased in leptin-deficient ob/ob mice. Strategies aimed at increasing GE should therefore be capable of improving glucose tolerance in these animals. The gut-derived hormone FGF19 has previously been shown to exert potent antidiabetic effects in ob/ob mice. In ob/ob mice, we found that systemic FGF19 administration improved glucose tolerance through its action in the brain and that a single, low-dose i.c.v. injection of FGF19 dramatically improved glucose intolerance within 2 hours. Minimal model analysis of glucose and insulin data obtained during a frequently sampled i.v. glucose tolerance test showed that the antidiabetic effect of i.c.v. FGF19 was solely due to increased GE and not to changes of either insulin secretion or insulin sensitivity. The mechanism underlying this effect appears to involve increased metabolism of glucose to lactate. Together, these findings implicate the brain in the antidiabetic action of systemic FGF19 and establish the brain’s capacity to rapidly, potently, and selectively increase insulin-independent glucose disposal. PMID:24084738

Morton, Gregory J.; Matsen, Miles E.; Bracy, Deanna P.; Meek, Thomas H.; Nguyen, Hong T.; Stefanovski, Darko; Bergman, Richard N.; Wasserman, David H.; Schwartz, Michael W.

2013-01-01

322

THE EFFECTS OF THE DIETARY GLYCEMIC LOAD ON GLUCOSE-INSULIN DYNAMICS AND SYSTEMIC INFLAMMATION IN A 6-MONTH RANDOMIZED CALORIC RESTRICTION TRIAL  

Technology Transfer Automated Retrieval System (TEKTRAN)

Insulin resistance, impaired beta cell function and systemic vascular inflammation are risk factors for glucose intolerance and type 2 diabetes. Diets low in glycemic load (GL) may improve these risk factors. Our objective was to compare the effects of two calorie-restricted diets that differ in gly...

323

Pulmonary hypertension in CKD.  

PubMed

Pulmonary arterial hypertension is a rare disease often associated with positive antinuclear antibody and high mortality. Pulmonary hypertension, which rarely is severe, occurs frequently in patients with chronic kidney disease (CKD). The prevalence of pulmonary hypertension ranges from 9%-39% in individuals with stage 5 CKD, 18.8%-68.8% in hemodialysis patients, and 0%-42% in patients on peritoneal dialysis therapy. No epidemiologic data are available yet for earlier stages of CKD. Pulmonary hypertension in patients with CKD may be induced and/or aggravated by left ventricular disorders and risk factors typical of CKD, including volume overload, an arteriovenous fistula, sleep-disordered breathing, exposure to dialysis membranes, endothelial dysfunction, vascular calcification and stiffening, and severe anemia. No specific intervention trial aimed at reducing pulmonary hypertension in patients with CKD has been performed to date. Correcting volume overload and treating left ventricular disorders are factors of paramount importance for relieving pulmonary hypertension in patients with CKD. Preventing pulmonary hypertension in this population is crucial because even kidney transplantation may not reverse the high mortality associated with established pulmonary hypertension. PMID:23164943

Bolignano, Davide; Rastelli, Stefania; Agarwal, Rajiv; Fliser, Danilo; Massy, Ziad; Ortiz, Alberto; Wiecek, Andrzej; Martinez-Castelao, Alberto; Covic, Adrian; Goldsmith, David; Suleymanlar, Gultekin; Lindholm, Bengt; Parati, Gianfranco; Sicari, Rosa; Gargani, Luna; Mallamaci, Francesca; London, Gerard; Zoccali, Carmine

2013-04-01

324

Hypertension in renal failure  

Microsoft Academic Search

Hypertension is a common component of the morbidity associated with renal failure. The mechanisms that contribute to high blood pressure are reviewed in this section. Also covered are therapies to reduce hypertension, the treatment goals of those therapies, and the outcomes of antihypertensive therapy on kidney function in patients with renal failure. Various antihypertensive agents are specifically addressed, and a

Michael Cirigliano

1998-01-01

325

Noncirrhotic Portal Hypertension  

PubMed Central

Portal hypertension is characterized by an increase in portal pressure (> 10 mmHg) and could be a result of cirrhosis of the liver or of noncirrhotic diseases. When portal hypertension occurs in the absence of liver cirrhosis, noncirrhotic portal hypertension (NCPH) must be considered. The prognosis of this disease is much better than that of cirrhosis. Noncirrhotic diseases are the common cause of portal hypertension in developing countries, especially in Asia. NCPH is a heterogeneous group of diseases that is due to intrahepatic or extrahepatic etiologies. In general, the lesions in NCPH are vascular in nature and can be classified based on the site of resistance to blood flow. In most cases, these disorders can be explained by endothelial cell lesions, intimal thickening, thrombotic obliterations, or scarring of the intrahepatic portal or hepatic venous circulation. Many different conditions can determine NCPH through the association of these various lesions in various degrees. Many clinical manifestations of NCPH result from the secondary effects of portal hypertension. Patients with NCPH present with upper gastrointestinal bleeding, splenomegaly, ascites after gastrointestinal bleeding, features of hypersplenism, growth retardation, and jaundice due to portal hypertensive biliopathy. Other sequelae include hyperdynamic circulation, pulmonary complications, and other effects of portosystemic collateral circulation like portosystemic encephalopathy. At present, pharmacologic and endoscopic treatments are the treatments of choice for portal hypertension. The therapy of all disorders causing NCPH involves the reduction of portal pressure by pharmacotherapy or portosystemic shunting, apart from prevention and treatment of complications of portal hypertension.

Rajekar, Harshal; Vasishta, Rakesh K; Chawla, Yogesh K; Dhiman, Radha K

2011-01-01

326

Lifestyle and hypertension  

Microsoft Academic Search

Lifestyle factors are critical determinants of blood pressure levels operating against a background of genetic susceptibility. Excess body fat is a predominant cause of hypertension with additive effects of dietary salt, alcohol, and physical inactivity. Controlled trials in hypertensives show blood pressure lowering effects of supplemental potassium, fibre, n-3 fatty acids, and diets rich in fruit and vegetables and low

L. J. Beilin; I. B. Puddey; V. Burke

1999-01-01

327

Childhood size is more strongly related than size at birth to glucose and insulin levels in 10–11-year-old children  

Microsoft Academic Search

Summary   In adults low birthweight and thinness at birth are associated with increased risk of glucose intolerance and non-insulin-dependent\\u000a diabetes mellitus. We have examined the relations between size at birth (birthweight, thinness at birth) and levels of plasma\\u000a glucose and serum insulin in children, and compared them with the effects of childhood size. We performed a school-based survey\\u000a of 10–11-year-old

P. H. Whincup; D. G. Cook; F. Adshead; S. J. C. Taylor; M. Walker; O. Papacosta; K. G. M. M. Alberti

1997-01-01

328

Emerging concepts in hypertension.  

PubMed

Cellular redox balance is vital in health and disease. In this Forum, we highlight the importance of reactive oxygen species (ROS) in the regulation of redox balance in different organ systems of the body and ROS contribution to the development of hypertension. The Forum examines interactions between oxidative and nitrosative stress in the brain, vasculature, and kidney, and redox effect on end-organ damage and hypertension. Furthermore, the Forum examines the role of immune cells in the modulation of hypertension. We also introduce a new role for endoplasmic reticulum stress in the induction of ROS and its possible contribution to the development of hypertension. Finally, we explore the clinical relevance of increased ROS in the setting of human hypertension. PMID:24392660

Francis, Joseph; Davisson, Robin L

2014-01-01

329

How Many People Are Affected or At Risk for Lactose Intolerance?  

MedlinePLUS

... African Americans Asian Americans Hispanic Americans Native Americans Lactose intolerance is uncommon in young children because most infants are born with enough lactase. But for many people, the amount of lactase ...

330

Fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) and nonallergic food intolerance: FODMAPs or food chemicals?  

PubMed Central

Food intolerance in irritable bowel syndrome (IBS) is increasingly being recognized, with patients convinced that diet plays a role in symptom induction. Evidence is building to implicate fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) in the onset of abdominal pain, bloating, wind and altered bowel habit through their fermentation and osmotic effects. Hypersensitivity to normal levels of luminal distension is known to occur in patients with IBS, with consideration of food chemical intolerance likely to answer many questions about this physiological process. This paper summarizes the evidence and application of the most common approaches to managing food intolerance in IBS: the low-FODMAP diet, the elimination diet for food chemical sensitivity and others including possible noncoeliac gluten intolerance. PMID:22778791

Gibson, Peter R.

2012-01-01

331

Novel epoxy activated hydrogels for solving lactose intolerance.  

PubMed

"Lactose intolerance" is a medical problem for almost 70% of the world population. Milk and dairy products contain 5-10%?w/v lactose. Hydrolysis of lactose by immobilized lactase is an industrial solution. In this work, we succeeded to increase the lactase loading capacity to more than 3-fold to 36.3?U/g gel using epoxy activated hydrogels compared to 11?U/g gel using aldehyde activated carrageenan. The hydrogel's mode of interaction was proven by FTIR, DSC, and TGA. The high activity of the epoxy group was regarded to its ability to attach to the enzyme's -SH, -NH, and -OH groups, whereas the aldehyde group could only bind to the enzyme's -NH2 group. The optimum conditions for immobilization such as epoxy chain length and enzyme concentration have been studied. Furthermore, the optimum enzyme conditions were also deliberated and showed better stability for the immobilized enzyme and the Michaelis constants, K m and V max, were doubled. Results revealed also that both free and immobilized enzymes reached their maximum rate of lactose conversion after 2?h, albeit, the aldehyde activated hydrogel could only reach 63% of the free enzyme. In brief, the epoxy activated hydrogels are more efficient in immobilizing more enzymes than the aldehyde activated hydrogel. PMID:25013804

Elnashar, Magdy M M; Hassan, Mohamed E

2014-01-01

332

Mechanisms of microgravity induced orthostatic intolerance: implications for effective countermeasures  

NASA Technical Reports Server (NTRS)

The development of orthostatic hypotension and instability immediately after return from spaceflight has been a significant operational problem to astronauts for more than four decades. Significant reductions in stroke volume and peripheral vascular resistance contribute to ineffective maintenance of systemic arterial blood pressure during standing after spaceflight despite compensatory elevations in heart rate. The primary mechanism underlying reduced stroke volume appears to be a reduction in preload associated with reduced circulating blood volume, although cardiac atrophy might also contribute. Space flight and ground based experiments have demonstrated that an inability to provide adequate peripheral vasoconstriction in astronauts that become presyncopal may be associated with several mechanisms including reduced sympathetic nerve activity, arterial smooth muscle atrophy and/or hyporeactivity, hypersensitivity of beta-adrenergic receptors, etc. In addition, an inability to provide adequate tachycardia in presyncopal subjects may be associated with reduced carotid-cardiac baroreflex sensitivity. Based on the current knowledge and understanding of cardiovascular mechanisms that are altered during exposure to microgravity, a major focus of future research should be directed to the systematic evaluation of potential countermeasures that specifically target and restore the function of these mechanisms. Based on a preliminary systematic evaluation presented in this review, acute physical exercise designed to elicit maximal effort, G-suit inflation, artificial gravity, and specific pharmacological interventions, alone or in combination, have shown promise as successful countermeasures that provide protection against post-flight orthostatic intolerance.

Convertino, Victor A.

2002-01-01

333

Pharmacological therapy of feed intolerance in the critically ills  

PubMed Central

Feed intolerance in the setting of critical illness is associated with higher morbidity and mortality, and thus requires promptly and effective treatment. Prokinetic agents are currently considered as the first-line therapy given issues relating to parenteral nutrition and post-pyloric placement. Currently, the agents of choice are erythromycin and metoclopramide, either alone or in combination, which are highly effective with relatively low incidence of cardiac, hemodynamic or neurological adverse effects. Diarrhea, however, can occur in up to 49% of patients who are treated with the dual prokinetic therapy, which is not associated with Clostridium difficile infection and settled soon after the cessation of the drugs. Hence, the use of prokinetic therapy over a long period or for prophylactic purpose must be avoided, and the indication for ongoing use of the drug(s) must be reviewed frequently. Second line therapy, such as total parenteral nutrition and post-pyloric feeding, must be considered once adverse effects relating the prokinetic therapy develop. PMID:25133043

Nguyen, Nam Q

2014-01-01

334

How to prevent intolerant agents from high segregation?  

E-print Network

In the framework of Agent-Based Complex Systems we examine dynamics that lead individuals towards spatial segregation. Such systems are constituted of numerous entities, among which local interactions create global patterns which cannot be easily related to the properties of the constituent entities. In the 70’s, Thomas C. Schelling showed that an important spatial segregation phenomenon may emerge at the global level, if it is based upon local preferences. Moreover, segregation may occur, even if it does not correspond to agent preferences. In real life preferences regarding segregation are influenced by individual contexts as well as social norms; in this paper we will propose a model which describes the dynamic evolution of individuals tolerance. We will introduce heterogeneity in agents ’ preferences and allow them to evolve over time. We will show that it is possible to dynamically get a distribution of tolerance over the agents with a low average and in the same time to deeply limit global aggregation. As the Schelling’s model showed that individual tolerance can nevertheless induce global aggregation, this paper takes the opposite view showing that intolerant agents can avoid segregation in some extent.

Salma Mesmoudi

335

Novel Epoxy Activated Hydrogels for Solving Lactose Intolerance  

PubMed Central

“Lactose intolerance” is a medical problem for almost 70% of the world population. Milk and dairy products contain 5–10%?w/v lactose. Hydrolysis of lactose by immobilized lactase is an industrial solution. In this work, we succeeded to increase the lactase loading capacity to more than 3-fold to 36.3?U/g gel using epoxy activated hydrogels compared to 11?U/g gel using aldehyde activated carrageenan. The hydrogel's mode of interaction was proven by FTIR, DSC, and TGA. The high activity of the epoxy group was regarded to its ability to attach to the enzyme's –SH, –NH, and –OH groups, whereas the aldehyde group could only bind to the enzyme's –NH2 group. The optimum conditions for immobilization such as epoxy chain length and enzyme concentration have been studied. Furthermore, the optimum enzyme conditions were also deliberated and showed better stability for the immobilized enzyme and the Michaelis constants, Km and Vmax, were doubled. Results revealed also that both free and immobilized enzymes reached their maximum rate of lactose conversion after 2?h, albeit, the aldehyde activated hydrogel could only reach 63% of the free enzyme. In brief, the epoxy activated hydrogels are more efficient in immobilizing more enzymes than the aldehyde activated hydrogel. PMID:25013804

Elnashar, Magdy M. M.; Hassan, Mohamed E.

2014-01-01

336

Angiogenic growth factors and hypertension  

Microsoft Academic Search

Emerging evidence supports a novel view of hypertension as a disease of inadequate or aberrant responses to angiogenic growth factors (AGF). Patients with hypertension have reduced microvascular density, with some evidence supporting a primary role for rarefaction in causing hypertension. Two clinical models have demonstrated a link between inhibition of AGF activity and hypertension. A major side effect of bevacizumab,

David C. Sane; Lauren Anton; K. Bridget Brosnihan

2004-01-01

337

Fructose and lactose intolerance and malabsorption testing: the relationship with symptoms in functional gastrointestinal disorders  

PubMed Central

Background The association of fructose and lactose intolerance and malabsorption with the symptoms of different functional gastrointestinal disorders (FGID) remains unclear. Aim To investigate the prevalence of fructose and lactose intolerance (symptom induction) and malabsorption and their association with clinical gastrointestinal (GI) as well as non-GI symptoms in FGID and the outcome of dietary intervention. Methods Fructose and lactose intolerance (defined by positive symptom index) and malabsorption (defined by increased hydrogen/methane) were determined in 1372 FGID patients in a single centre using breath testing. Results were correlated with clinical symptoms in different FGID Rome III subgroups. The effectiveness of a targeted saccharide-reduced diet was assessed after 6–8 weeks. Results Intolerance prevalence across all FGIDs was 60% to fructose, 51% to lactose and 33% to both. Malabsorption occurred in 45%, 32% and 16% respectively. There were no differences in intolerance or malabsorption prevalence between FGID subgroups. FGID symptoms correlated with symptoms evoked during testing (r = 0.35–0.61. P < 0.0001), but not with malabsorption. Non-GI symptoms occurred more commonly in patients with intolerances. Methane breath levels were not associated with constipation using several cut-off thresholds. Adequate symptom relief was achieved in >80% of intolerant patients, irrespective of malabsorption. Conclusions Fructose and lactose intolerances are common in FGID and associated with increased non-GI symptoms, but not with specific FGID subtypes. Symptoms experienced during breath testing, but not malabsorption, correlate with FGID symptoms. Effective symptom relief with dietary adaptation is not associated with malabsorption. Mechanisms relating to the generation of GI and non-GI symptoms due to lactose and fructose in FGID need to be explored further. PMID:23574302

Wilder-Smith, C H; Materna, A; Wermelinger, C; Schuler, J

2013-01-01

338

Leukocyte interferon-? and ribavirin for treatment of chronic hepatitis C patients intolerant to pegylated-interferon  

Microsoft Academic Search

Treatments for chronic hepatitis C (CHC) patients intolerant to pegylated interferons (peg-IFNs) are lacking. Thus, such patients\\u000a remain at high risk of developing an advanced and decompensated liver disease. Leukocyte IFN-? (Le-IFN-?) seems to possess\\u000a a safer profile than other natural and recombinant ?-interferons, but no information is available for peg-IFN intolerant patients.\\u000a Accordingly, we evaluated the safety and efficacy

Luigi E. Adinolfi; Emanuele Durante-Mangoni; Marta Salzillo; Aldo Marrone; Marie-Francoise Tripodi; Luciano Restivo; Antonietta Merola; Rosa Zampino; Giuseppe Ruggiero

2009-01-01

339

Syncope and orthostatic intolerance increase risk of brain lesions in migraineurs and controls  

PubMed Central

Objectives: We and others showed that migraineurs are at increased risk of subclinical and clinical ischemic brain lesions. Migraineurs also have a higher prevalence of frequent syncope and orthostatic intolerance, symptoms that are associated with transient reductions in cerebral blood flow. In this study, we assessed whether these autonomic symptoms may contribute to the increased risk of brain lesions in migraine. Methods: Migraineurs (n = 291) and controls (n = 140) from the population-based, cross-sectional CAMERA (Cerebral Abnormalities in Migraine, an Epidemiologic Risk Analysis) cohort (aged 30–60 years, and free of other neurologic symptoms) underwent 1) brain MRI scan, and 2) structured telephone interview including questions on frequent syncope (?5/lifetime) and orthostatic intolerance. Results: Frequent syncope (odds ratio [OR] = 2.7; 95% confidence interval: 1.3–5.5) and orthostatic intolerance (OR = 2.0 [1.1–3.6]) were independent risk factors for high load of deep white matter lesions. Effects were strongest in women and similar in migraineurs and controls. Migraine diagnosis did not mediate or moderate these associations. Individuals with orthostatic intolerance had higher prevalence of high periventricular white matter lesion load (OR = 1.9 [1.1–3.5]). Syncope and orthostatic intolerance were not related to subclinical infarcts or infratentorial lesions. Conclusions: Frequent syncope, orthostatic intolerance, and migraine independently increase the risk of white matter lesions, particularly in females. PMID:23616159

Thijs, Roland D.; Ferrari, Michel D.; Launer, Lenore J.; van Buchem, Mark A.; van Dijk, J. Gert

2013-01-01

340

Fear of heights and mild visual height intolerance independent of alcohol consumption  

PubMed Central

Background Visual height intolerance occurs when a visual stimulus causes apprehension of losing balance and falling from some height. Affecting one-third of the population, it has a broad spectrum of symptoms, ranging from minor distress to fear of heights, which is defined as a specific phobia. Specific phobias are associated with higher alcohol consumption. This has not been specifically shown for susceptibility to the more general visual height intolerance. Methods Representative case–control study nested within a population-based cross-sectional telephone survey to assess epidemiologically 1253 individuals ?14 years, using a questionnaire on sociodemographic data, typical symptoms, precipitating visual stimuli, and alcohol drinking patterns (overall frequency of alcohol consumption, the daily quantities, and the motives). Results Individuals susceptible or nonsusceptible to visual height intolerance showed no significant differences in drinking patterns. The daily average alcohol consumption was slightly higher in persons susceptible to visual height intolerance (4.1 g/day vs. 3.7 g/day). Of those consuming alcohol, cases and controls reported on average consuming 2.3 glasses per day. The prevalence of visual height intolerance was insignificantly higher in the small minority of those drinking 2–3 times per week versus teetotalers. Conclusions Our study does not provide evidence that visual height intolerance – contrary to various specific phobias – is significantly associated with individual alcohol consumption patterns. PMID:24392279

Huppert, Doreen; Grill, Eva; Kapfhammer, Hans-Peter; Brandt, Thomas

2013-01-01

341

Histamine 50-Skin-Prick Test: A Tool to Diagnose Histamine Intolerance  

PubMed Central

Background. Histamine intolerance results from an imbalance between histamine intake and degradation. In healthy persons, dietary histamine can be sufficiently metabolized by amine oxidases, whereas persons with low amine oxidase activity are at risk of histamine toxicity. Diamine oxidase (DAO) is the key enzyme in degradation. Histamine elicits a wide range of effects. Histamine intolerance displays symptoms, such as rhinitis, headache, gastrointestinal symptoms, palpitations, urticaria and pruritus. Objective. Diagnosis of histamine intolerance until now is based on case history; neither a validated questionnaire nor a routine test is available. It was the aim of this trial to evaluate the usefullness of a prick-test for the diagnosis of histamine intolerance. Methods. Prick-testing with 1% histamine solution and wheal size-measurement to assess the relation between the wheal in prick-test, read after 20 to 50 minutes, as sign of slowed histamine degradation as well as history and symptoms of histamine intolerance. Results. Besides a pretest with 17 patients with HIT we investigated 156 persons (81 with HIT, 75 controls): 64 out of 81 with histamine intolerance(HIT), but only 14 out of 75 persons from the control-group presented with a histamine wheal ?3?mm after 50 minutes (P < .0001). Conclusion and Clinical Relevance. Histamine-50 skin-prickt-test offers a simple tool with relevance. PMID:23724226

Kofler, Lukas; Ulmer, Hanno; Kofler, Heinz

2011-01-01

342

An examination of distress intolerance in undergraduate students high in symptoms of generalized anxiety disorder.  

PubMed

People with generalized anxiety disorder (GAD) engage in maladaptive coping strategies to reduce or avoid distress. Evidence suggests that uncertainty and negative emotions are triggers for distress in people with GAD; however, there may also be other triggers. Recent conceptualizations have highlighted six types of experiences that people report having difficulty withstanding: uncertainty, negative emotions, ambiguity, frustration, physical discomfort, and the perceived consequences of anxious arousal. The present study examined the extent to which individuals high in symptoms of GAD are intolerant of these distress triggers, compared to individuals high in depressive symptoms, and individuals who are low in GAD and depressive symptoms. Undergraduate students (N = 217) completed self-report measures of GAD symptoms, depressive symptoms, and distress intolerance. Individuals high in GAD symptoms reported greater intolerance of all of the distress triggers compared to people low in symptoms of GAD and depression. Individuals high in GAD symptoms reported greater intolerance of physical discomfort compared to those high in depressive symptoms. Furthermore, intolerance of physical discomfort was the best unique correlate of GAD status, suggesting that it may be specific to GAD (versus depression). These findings support continued investigation of the transdiagnosticity and specificity of distress intolerance. PMID:25299853

MacDonald, Emma M; Pawluk, Elizabeth J; Koerner, Naomi; Goodwill, Alasdair M

2015-01-01

343

Hypothalamic signaling mechanisms in hypertension.  

PubMed

The etiology of hypertension, a critical public health issue affecting one in three US adults, involves the integration of the actions of multiple organ systems, including the central nervous system. Increased activation of the central nervous system, driving enhanced sympathetic outflow and increased blood pressure, has emerged as a major contributor to the pathogenesis of hypertension. The hypothalamus is a key brain site acting to integrate central and peripheral inputs to ultimately impact blood pressure in multiple disease states that evoke hypertension. This review highlights recent advances that have identified novel signal transduction mechanisms within multiple hypothalamic nuclei (e.g., paraventricular nucleus, arcuate nucleus) acting to drive the pathophysiology of hypertension in neurogenic hypertension, angiotensin II hypertension, salt-sensitive hypertension, chronic intermittent hypoxia, and obesity-induced hypertension. Increased understanding of hypothalamic activity in hypertension has the potential to identify novel targets for future therapeutic interventions designed to treat hypertension. PMID:25860531

Carmichael, Casey Y; Wainford, Richard D

2015-05-01

344

Glucose Metabolism and Pancreatic Defects in Spinal Muscular Atrophy  

PubMed Central

Objective Spinal muscular atrophy (SMA) is the number 1 genetic killer of young children. It is caused by mutation or deletion of the survival motor neuron 1 (SMN1) gene. Although SMA is primarily a motor neuron disease, metabolism abnormalities such as metabolic acidosis, abnormal fatty acid metabolism, hyperlipidemia, and hyperglycemia have been reported in SMA patients. We thus initiated an in-depth analysis of glucose metabolism in SMA. Methods Glucose metabolism and pancreas development were investigated in the Smn2B/? intermediate SMA mouse model and type I SMA patients. Results Here, we demonstrate in an SMA mouse model a dramatic cell fate imbalance within pancreatic islets, with a predominance of glucagon-producing ? cells at the expense of insulin-producing ? cells. These SMA mice display fasting hyperglycemia, hyperglucagonemia, and glucose resistance. We demonstrate similar abnormalities in pancreatic islets from deceased children with the severe infantile form of SMA in association with supportive evidence of glucose intolerance in at least a subset of such children. Interpretation Our results indicate that defects in glucose metabolism may play an important contributory role in SMA pathogenesis. PMID:22926856

Bowerman, Melissa; Swoboda, Kathryn J.; Michalski, John-Paul; Wang, Gen-Sheng; Reeks, Courtney; Beauvais, Ariane; Murphy, Kelley; Woulfe, John; Screaton, Robert A.; Scott, Fraser W.; Kothary, Rashmi

2014-01-01

345

Pseudohyperaldosteronism, liquorice, and hypertension.  

PubMed

Consumption of large quantities of liquorice can cause hypokalemia and hypertension. These effects are associated with increased cortisol-mediated activation of renal mineralocorticoid receptors and hypoaldosteronism. The authors describe a patient with long-standing hypokalemia and uncontrolled hypertension related to excessive ingestion of liquorice. The case highlights the importance of obtaining a detailed dietary history, especially considering the increasing use of liquorice-containing foods, teas, and herbal products. The authors also discuss secondary causes of hypertension, focusing on pseudohyperaldosteronism. PMID:18256580

Sontia, Bruno; Mooney, Jan; Gaudet, Lise; Touyz, Rhian M

2008-02-01

346

Perioperative hypertension management  

PubMed Central

Perioperative hypertension is commonly encountered in patients that undergo surgery. While attempts have been made to standardize the method to characterize the intraoperative hemodynamics, these methods still vary widely. In addition, there is a lack of consensus concerning treatment thresholds and appropriate therapeutic targets, making absolute recommendations about treatment difficult. Nevertheless, perioperative hypertension requires careful management. When treatment is necessary, therapy should be individualized for the patient. This paper reviews the pharmacologic agents and strategies commonly used in the management of perioperative hypertension. PMID:18827911

Varon, Joseph; Marik, Paul E

2008-01-01

347

Management of Intracranial Hypertension  

PubMed Central

Effective management of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased intracranial pressure. When intracranial pressure becomes elevated, it is important to rule out new mass lesions that should be surgically evacuated. Medical management of increased intracranial pressure should include sedation, drainage of cerebrospinal fluid, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension resulting from traumatic brain injury. PMID:18514825

Rangel-Castillo, Leonardo; Gopinath, Shankar; Robertson, Claudia S.

2008-01-01

348

PKA Enhances the Acute Insulin Response Leading to the Restoration of Glucose Control.  

PubMed

Diabetes arises from insufficient insulin secretion and failure of the ?-cell mass to persist and expand. These deficits can be treated with ligands to Gs-coupled G-protein-coupled receptors that raise ?-cell cAMP. Here we studied the therapeutic potential of ?-cell cAMP-dependent protein kinase (PKA) activity in restoring glucose control using ?-caPKA mice. PKA activity enhanced the acute insulin response (AIR) to glucose, which is a primary determinant of the efficacy of glucose clearance. Enhanced AIR improved peripheral insulin action, leading to more rapid muscle glucose uptake. In the setting of pre-established glucose intolerance caused by diet-induced insulin resistance or streptozotocin-mediated ?-cell mass depletion, PKA activation enhanced ?-cell secretory function to restore glucose control, primarily through augmentation of the AIR. Enhanced AIR and improved glucose control were maintained through 16 weeks of a high-fat diet and aging to 1 year. Importantly, improved glucose tolerance did not increase the risk for hypoglycemia, nor did it rely upon hyperinsulinemia or ?-cell hyperplasia, although PKA activity was protective for ?-cell mass. These data highlight that improving ?-cell function through the activation of PKA has a large and underappreciated capacity to restore glucose control with minimal risk for adverse side effects. PMID:25475437

Kaihara, Kelly A; Dickson, Lorna M; Ellenbroek, Johanne H; Orr, Caitlin M D; Layden, Brian T; Wicksteed, Barton

2015-05-01

349

Natural sweetening of food products by engineering Lactococcus lactis for glucose production.  

PubMed

We show that sweetening of food products by natural fermentation can be achieved by a combined metabolic engineering and transcriptome analysis approach. A Lactococcus lactis ssp. cremoris strain was constructed in which glucose metabolism was completely disrupted by deletion of the genes coding for glucokinase (glk), EII(man/glc) (ptnABCD), and the newly discovered glucose-PTS EII(cel) (ptcBAC). After introducing the lactose metabolic genes, the deletion strain could solely ferment the galactose moiety of lactose, while the glucose moiety accumulated extracellularly. Additionally, less lactose remained in the medium after fermentation. The resulting strain can be used for in situ production of glucose, circumventing the need to add sweeteners as additional ingredients to dairy products. Moreover, the enhanced removal of lactose achieved by this strain could be very useful in the manufacture of products for lactose intolerant individuals. PMID:16844396

Pool, Wietske A; Neves, Ana Rute; Kok, Jan; Santos, Helena; Kuipers, Oscar P

2006-09-01

350

Pancreatic resection: effects on glucose metabolism.  

PubMed

Pancreatic resection results in hormonal abnormalities that are dependent on the extent and location (proximal versus distal) of the resected portion of the gland. The form of glucose intolerance which results from pancreatic resection is termed pancreatogenic diabetes. It is associated with features distinct from both type I (insulin-dependent) and type II (insulin-independent, or adult-onset) diabetes. Hepatic insulin resistance with persistent endogenous glucose production and enhanced peripheral insulin sensitivity result in a brittle form of diabetes which can be difficult to manage. In addition to insulin deficiency, the endocrine abnormalities that accompany pancreatic resection can include glucagon deficiency or pancreatic polypeptide (PP) deficiency if the resection is distal or proximal, respectively. Glucagon deficiency can contribute to iatrogenic hypoglycemia, and PP deficiency can contribute to persistent hyperglycemia due to impaired hepatic insulin action. Pancreatic resections that spare the duodenum, such as distal pancreatectomy, duodenum-preserving pancreatic head resection (Beger procedure), or extended lateral pancreaticojejunostomy with excavation of the pancreatic head (Frey procedure), are associated with a lower incidence of new or worsened diabetes than the standard or pylorus-preserving pancreaticoduodenectomy (Whipple procedure) or total pancreatectomy. Operative considerations for the treatment of pancreatic disease should include strategies to minimize the hormonal impairment of pancreatic resection. PMID:11344398

Slezak, L A; Andersen, D K

2001-04-01

351

Improving hypertension self-management with community health coaches.  

PubMed

Approximately two thirds of those older than 60 years have a hypertension diagnosis. The aim of our program, Health Coaches for Hypertension Control, is to improve hypertension self-management among rural residents older than 60 years through education and support offered by trained community volunteers called Health Coaches. Participants received baseline and follow-up health risk appraisals with blood work, educational materials, and items such as blood pressure monitors and pedometers. Data were collected at baseline, 8 weeks, and 16 weeks on 146 participants who demonstrated statistically significant increases in hypertension-related knowledge from baseline to 8 weeks that persisted at 16 weeks, as well as significant improvements in stage of readiness to change behaviors and in actual behaviors. Furthermore, clinically significant decreases in all outcome measures were observed, with statistically significant changes in systolic blood pressure (-5.781 mmHg; p = .001), weight (-2.475 lb; p < .001), and glucose (-5.096 mg/dl; p = .004) after adjusting for multiple comparisons. Although 40.4% of participants met the Healthy People 2020 definition of controlled hypertension at baseline, the proportion of participants meeting this definition at 16 weeks postintervention increased to 51.0%. This article describes a university-community-hospital system model that effectively promotes hypertension self-management in a rural Appalachian community. PMID:24837989

Dye, Cheryl J; Williams, Joel E; Evatt, Janet Hoffman

2015-03-01

352

Continuous Glucose Monitoring  

MedlinePLUS

... How does CGM compare with standard blood glucose tests? Studies show that both short- and long-term ... try CGM. Sometimes the standard blood glucose meter tests miss large and long-lasting ups and downs ...

353

PROX1 GENE VARIANT IS ASSOCIATED WITH FASTING GLUCOSE CHANGE AFTER ANTIHYPERTENSIVE TREATMENT  

PubMed Central

Study Objective To assess the relationship of the 33 single nucleotide polymorphisms (SNPs) previously associated with fasting glucose in Caucasians in genome-wide association studies (GWAS) with glucose response to antihypertensive drugs shown to increase risk for hyperglycemia and diabetes. Design Randomized, multicenter clinical trial. Subjects A total of 456 Caucasian men and women with uncomplicated hypertension Measurements and Main Results The Pharmacogenomic Evaluation of Antihypertensives Responses study evaluated blood pressure and glucose response in uncomplicated hypertensive patients randomized to either atenolol or hydrochlorothiazide (HCTZ) monotherapy, followed by combination therapy with both agents. Association of these SNPs with atenolol- or HCTZ-induced glucose response was evaluated in 456 Caucasian patients using linear regression adjusting for age, gender, body mass index, baseline glucose, baseline insulin, and principal component for ancestry. SNP rs340874 in the 5’ region of PROX1 gene was significantly associated with atenolol-induced glucose change (p=0.0013). Participants harboring the C allele of this SNP had greater glucose elevation after approximately 9 weeks of atenolol monotherapy (beta = +2.39 mg/dL per C allele), consistent with the direction of effect in fasting glucose GWAS that C allele is associated with higher fasting glucose. Conclusion These data suggest that PROX1 SNP rs340874 discovered in fasting glucose GWAS may also be a pharmacogenetic risk factor for antihypertensive - induced hyperglycemia. ?-blockers and thiazides may interact with genetic risk factors to increase risk for dysglycemia and diabetes. PMID:24122840

Gong, Yan; McDonough, Caitrin W; Beitelshees, Amber L; Karnes, Jason H; O’Connell, Jeffrey R.; Turner, Stephen T; Chapman, Arlene B; Gums, John G; Bailey, Kent R; Boerwinkle, Eric; Johnson, Julie A; Cooper-DeHoff, Rhonda M

2013-01-01

354

Hypertensive heart disease  

MedlinePLUS

... failure: pathophysiology and diagnosis. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine . 24th ed. Philadelphia, PA: ... Victor RG. Arterial hypertension. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine . 24th ed. Philadelphia, PA: ...

355

High Blood Pressure (Hypertension)  

MedlinePLUS

... Text Size: A A A Listen High Blood Pressure (Hypertension) Nearly 1 in 3 American adults has ... your doctor prescribes it, medicine. What Is Blood Pressure? Blood pressure is the force of blood flow ...

356

High Blood Pressure (Hypertension)  

MedlinePLUS

... Consumer Information by Audience For Women High Blood Pressure (Hypertension) Print and Share (PDF 109 KB) En ... Who is at risk? How is high blood pressure treated? Understanding your blood pressure: What do the ...

357

Molecular Structure of Glucose  

NSDL National Science Digital Library

Glucose is named after a Greek word meaning sugar or sweet. One of the most important compounds to life, glucose was first discovered by Andreas Marggraf in 1747. The structure for glucose was first discovered by Emil Fischer during the late 19th century and early 20th century. Glucose is found in all life forms and is used as a means of storing energy. When it polymerizes, it forms cellulose, which comprises plant structures.

2002-08-13

358

Management of hypertension emergencies  

Microsoft Academic Search

Although they have become less common, hypertensive emergencies occur with an incidence of approximately 1 to 2\\/100,000 people\\u000a per year. Our knowledge about this problem, its pathophysiology, risk factors, and appropriate treatment options has expanded\\u000a during the past decade. A hypertensive emergency can be declared when an elevated blood pressure is associated with acute\\u000a targetorgan damage. Rapid evaluation and treatment

William J. Elliott

2003-01-01

359

Pharmacotherapy of Pulmonary Hypertension  

PubMed Central

Pulmonary arterial hypertension is a serious disease with significant morbidity and mortality. While it can occur idiopathically, it is more commonly associated with other cardiac or lung diseases. While most of the available therapies were tested in adult populations, and most therapies in children remain off-label, new reports and randomized trials are emerging that inform the treatment of pediatric populations. This review discusses currently available therapies for pediatric pulmonary hypertension, their biologic rationales, and evidence for their clinical effectiveness. PMID:23036248

Steinhorn, Robin H.

2012-01-01

360

Chronic Thromboembolic Pulmonary Hypertension  

Microsoft Academic Search

Chronic thromboembolic pulmonary hypertension (CTEPH) is an important form of pulmonary hypertension to detect because prompt\\u000a treatment can lead to a surgical cure. The true incidence is unknown, but it is estimated to occur in 1% to 3% of patients\\u000a following acute thromboembolism. Detection may be difficult, because symptoms are nonspecific and other diagnoses are often\\u000a made before that of

William R. Auger; Peter F. Fedullo

361

Dopaminergic defect in hypertension.  

PubMed

Reverse genetics and the candidate gene approach have been utilized to identify the genetic defect(s) in hypertension. We have proposed the dopamine receptor gene as one candidate in the pathogenesis of hypertension. Because some forms of hypertension are sodium dependent or aggravated by sodium loading and because dopamine is important in aiding the organism to eliminate "excess" sodium, an abnormality in the renal dopaminergic system may be responsible for the sodium retention in hypertension. Both human and animal models of hypertension are associated with renal dopamine production and/or post first messenger defects. The Dahl salt-sensitive rat, which has a decreased ability to generate renal dopamine, and the spontaneously hypertensive rat (SHR), which has no such limitation, have a defective coupling of a D1 receptor to a G protein/adenylyl cyclase complex. This coupling defect is: (1) genetic, since it precedes the onset of hypertension and co-segregates with the hypertensive phenotype, (2) receptor specific, since it is not shared by other humoral agents, and (3) organ and nephron segment selective, since it occurs in proximal tubules but not in cortical collecting ducts or the brain striatum. A consequence of the defective dopamine receptor/adenylyl cyclase coupling in the SHR is a decreased ability of D1 agonists to inhibit Na+/H+ exchange activity. A resistance to the natriuretic effect of dopamine and D1 agonists in the SHR is due mainly to decreased cyclic AMP production, although with maturation a post cyclic AMP defect is acquired. Radioligand binding studies suggest a "loss" of the high-affinity D1 binding site in the SHR.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:8130121

Jose, P A; Eisner, G M; Felder, R A

1993-12-01

362

Utility of Corrected QT Interval in Orthostatic Intolerance  

PubMed Central

We performed this study to determine whether electrocardiographic corrected QT (QTc) interval predicts alterations in sympathovagal balance during orthostatic intolerance (OI). We reviewed 1,368 patients presenting with symptoms suggestive of OI who underwent electrocardiography and composite autonomic function tests (AFTs). Patients with a positive response to the head-up tilt test were classified into orthostatic hypotension (OH), neurocardiogenic syncope (NCS), or postural orthostatic tachycardia syndrome (POTS) groups. A total of 275 patients (159 OH, 54 NCS, and 62 POTS) were included in the final analysis. Between-group comparisons of OI symptom grade, QTc interval, QTc dispersion, and each AFT measure were performed. QTc interval and dispersion were correlated with AFT measures. OH Patients had the most severe OI symptom grade and NCS patients the mildest. Patients with OH showed the longest QTc interval (448.8±33.6 msec), QTc dispersion (59.5±30.3 msec) and the lowest values in heart rate response to deep breathing (HRDB) (10.3±6.0 beats/min) and Valsalva ratio (1.3±0.2). Patients with POTS showed the shortest QTc interval (421.7±28.6 msec), the highest HRDB values (24.5±9.2 beats/min), Valsalva ratio (1.8±0.3), and proximal and distal leg sweat volumes in the quantitative sudomotor axon reflex test. QTc interval correlated negatively with HRDB (r?=??0.443, p<0.001) and Valsalva ratio (r?=??0.425, p<0.001). We found negative correlations between QTc interval and AFT values representing cardiovagal function in patients with OI. Our findings suggest that prolonged QTc interval may be considered to be a biomarker for detecting alterations in sympathovagal balance, especially cardiovagal dysfunction in OH. PMID:25180969

Kim, Jung Bin; Hong, Soonwoong; Park, Jin-Woo; Cho, Dong-Hyuk; Park, Ki-Jong; Kim, Byung-Jo

2014-01-01

363

Utility of corrected QT interval in orthostatic intolerance.  

PubMed

We performed this study to determine whether electrocardiographic corrected QT (QTc) interval predicts alterations in sympathovagal balance during orthostatic intolerance (OI). We reviewed 1,368 patients presenting with symptoms suggestive of OI who underwent electrocardiography and composite autonomic function tests (AFTs). Patients with a positive response to the head-up tilt test were classified into orthostatic hypotension (OH), neurocardiogenic syncope (NCS), or postural orthostatic tachycardia syndrome (POTS) groups. A total of 275 patients (159 OH, 54 NCS, and 62 POTS) were included in the final analysis. Between-group comparisons of OI symptom grade, QTc interval, QTc dispersion, and each AFT measure were performed. QTc interval and dispersion were correlated with AFT measures. OH Patients had the most severe OI symptom grade and NCS patients the mildest. Patients with OH showed the longest QTc interval (448.8±33.6 msec), QTc dispersion (59.5±30.3 msec) and the lowest values in heart rate response to deep breathing (HRDB) (10.3±6.0 beats/min) and Valsalva ratio (1.3±0.2). Patients with POTS showed the shortest QTc interval (421.7±28.6 msec), the highest HRDB values (24.5±9.2 beats/min), Valsalva ratio (1.8±0.3), and proximal and distal leg sweat volumes in the quantitative sudomotor axon reflex test. QTc interval correlated negatively with HRDB (r?=?-0.443, p<0.001) and Valsalva ratio (r?=?-0.425, p<0.001). We found negative correlations between QTc interval and AFT values representing cardiovagal function in patients with OI. Our findings suggest that prolonged QTc interval may be considered to be a biomarker for detecting alterations in sympathovagal balance, especially cardiovagal dysfunction in OH. PMID:25180969

Kim, Jung Bin; Hong, Soonwoong; Park, Jin-Woo; Cho, Dong-Hyuk; Park, Ki-Jong; Kim, Byung-Jo

2014-01-01

364

Cerebral vasoconstriction precedes orthostatic intolerance after parabolic flight.  

PubMed

The effects of brief but repeated bouts of micro- and hypergravity on cerebrovascular responses to head-up tilt (HUT) were examined in 13 individuals after (compared to before) parabolic flight. Middle cerebral artery mean flow velocity (MCA MFV; transcranial Doppler ultrasound), eye level blood pressure (BP) and end tidal CO(2) (P(ET)CO(2)) were measured while supine and during 80 degrees HUT for 30 min or until presyncope. In the postflight tests subjects were classified as being orthostatically tolerant (OT) (n = 7) or intolerant (OI) (n = 6). BP was diminished with HUT in the OT group in both tests (p < 0.05) whereas postflight BP was not different from supine in the OI group. Postflight compared to preflight, the reduction in P(ET)CO(2) with HUT (p < 0.05) increased in both groups, although significantly so only in the OI group (p < 0.05). The OI group also had a significant decrease in supine MCA MFV postflight (p < 0.05) that was unaccompanied by a change in supine P(ET)CO(2). The decrease in MCA MFV that occurred during HUT in both groups preflight (p < 0.05) was accentuated only in the OI group postflight, particularly during the final 30 s of HUT (p < 0.05). However, this accentuated decrease in MCA MFV was not correlated to the greater decrease in P(ET)CO(2) during the same period (R = 0.20, p = 0.42). Although cerebral vascular resistance (CVR) also increased in the OI group during the last 30 s of HUT postflight (p < 0.05), the dynamic autoregulatory gain was not simultaneously changed. Therefore, we conclude that in the OI individuals, parabolic flight was associated with cerebral hypoperfusion following a paradoxical augmentation of CVR by a mechanism that was not related to changes in autoregulation nor strictly to changes in P(ET)CO(2). PMID:11033215

Serrador, J M; Shoemaker, J K; Brown, T E; Kassam, M S; Bondar, R L; Schlegel, T T

2000-09-01

365

Visual height intolerance and acrophobia: clinical characteristics and comorbidity patterns.  

PubMed

The purpose of this study was to estimate the general population lifetime and point prevalence of visual height intolerance and acrophobia, to define their clinical characteristics, and to determine their anxious and depressive comorbidities. A case-control study was conducted within a German population-based cross-sectional telephone survey. A representative sample of 2,012 individuals aged 14 and above was selected. Defined neurological conditions (migraine, Menière's disease, motion sickness), symptom pattern, age of first manifestation, precipitating height stimuli, course of illness, psychosocial impairment, and comorbidity patterns (anxiety conditions, depressive disorders according to DSM-IV-TR) for vHI and acrophobia were assessed. The lifetime prevalence of vHI was 28.5 % (women 32.4 %, men 24.5 %). Initial attacks occurred predominantly (36 %) in the second decade. A rapid generalization to other height stimuli and a chronic course of illness with at least moderate impairment were observed. A total of 22.5 % of individuals with vHI experienced the intensity of panic attacks. The lifetime prevalence of acrophobia was 6.4 % (women 8.6 %, men 4.1 %), and point prevalence was 2.0 % (women 2.8 %; men 1.1 %). VHI and even more acrophobia were associated with high rates of comorbid anxious and depressive conditions. Migraine was both a significant predictor of later acrophobia and a significant consequence of previous acrophobia. VHI affects nearly a third of the general population; in more than 20 % of these persons, vHI occasionally develops into panic attacks and in 6.4 %, it escalates to acrophobia. Symptoms and degree of social impairment form a continuum of mild to seriously distressing conditions in susceptible subjects. PMID:25262317

Kapfhammer, Hans-Peter; Huppert, Doreen; Grill, Eva; Fitz, Werner; Brandt, Thomas

2014-09-28

366

Home blood glucose monitoring  

Microsoft Academic Search

Conclusion  Doctors find it impossible to stabilize and monitor diabetic patients in hospital without measuring blood glucose levels and it seemed logical that patients would also manage themselves better if they were able to measure blood glucose during their ordinary life. The development of glucose oxidase sticks and Reflectance meters has made this possible. Six groups have published their experience with

R. B. Tattersall

1979-01-01

367

Alpha 1-blocker combination therapy for hypertension.  

PubMed

Combination therapy is a cost-effective and rational approach to treatment of severe hypertension and of mild to moderate hypertension that is refractory to monotherapy. The method has several advantages, most notably improved tolerability and enhanced antihypertensive efficacy. Long-term prospective studies are needed to confirm that such agents as calcium channel blockers, ACE inhibitors, and alpha 1 blockers reduce end-organ damage more effectively than do older antihypertensive drugs. However, scientific evidence strongly suggests that reducing risk factors for end-organ damage reduces heart, brain, kidney, and large-artery injury. Alpha 1 blockers appear to be a particularly suitable choice for use in combination regimens. The only class of agents that should be avoided in combination with alpha 1 blockers is central alpha agonists; all other agents act in an additive or synergistic fashion. Unlike diuretics and beta blockers, alpha 1 blockers do not adversely affect serum lipid, glucose, or insulin levels. In fact, alpha 1 blockers may improve these measurements and also counteract the adverse effects of other antihypertensive agents on them. Alpha1-blocker therapy may bring about regression of LVH, and it does not have deleterious effects on disorders that often coexist with hypertension (e.g., gout, chronic obstructive lung disease, peripheral ischemia). PMID:9742910

Houston, M C

1998-09-01

368

Novel treatment approaches in hypertensive type 2 diabetic patients  

PubMed Central

Type 2 diabetes mellitus (T2DM) and hypertension represent two common conditions worldwide. Their frequent association with cardiovascular diseases makes management of hypertensive patients with T2DM an important clinical priority. Carvedilol and renal denervation are two promising choices to reduce plasma glucose levels and blood pressure in hypertensive patients with T2DM to reduce future complications and improve clinical outcomes and prognosis. Pathophysiological mechanisms of both options are under investigation, but one of the most accepted is an attenuation in sympathetic nervous system activity which lowers blood pressure and improves insulin sensitivity. Choice of these therapeutic approaches should be individualized based on specific characteristics of each patient. Further investigations are needed to determine when to consider their use in clinical practice. PMID:25126399

Castro Torres, Yaniel; Katholi, Richard E

2014-01-01

369

Insulin Sensitivity and Beta-Cell Function Are Associated with Arterial Stiffness in Individuals without Hypertension  

PubMed Central

Aim. We investigated the relationship between brachial-ankle pulse wave velocity (baPWV) and glucose levels, insulin sensitivity, and beta-cell function in Chinese individuals with or without hypertension. Methods. We recruited 3137 nondiabetic individuals whose age, body mass index (BMI), glucose levels, blood pressure (BP), lipids, hemoglobin A1C (HbA1c), baPWV, and insulin levels were measured. Results. In normotensive group, 2?h glucose levels (? = 0.046, P < 0.001) associated with baPWV, showed a significant increase in patients with NG as compared to those with DM (P = 0.032). The hypertensive group showed no such differences. The Matsuda index (? = 0.114, P < 0.001) and HOMA-? (? = 0.045, P < 0.001) were negatively correlated with baPWV while lnHOMA-IR (? = 0.196, P = 0.076) and the Quantitative Insulin Sensitivity Check Index (QUICKI) (? = 0.226, P = 0.046) showed a borderline negative correlation. BaPWV significantly decreased (P = 0.032) with an increase in insulin sensitivity in individuals with both normal BP and glucose tolerance. Conclusions. BaPWV was significantly associated with 2?h glucose levels, insulin sensitivity and beta-cell function in normotensive population, whereas in hypertensive individuals, BP was the dominant factor influencing arterial stiffness. Individuals with abnormal insulin sensitivity in the absence of diabetes and hypertension are also at an increased risk of arterial stiffness. PMID:23671853

Meng, Chuchen; Sun, Min; Wang, Zhixiao; Fu, Qi; Cao, Mengdie; Zhu, Zhenxin; Mao, Jia; Shi, Yun; Tang, Wei; Huang, Xiaoping; Duan, Yu; Yang, Tao

2013-01-01

370

Relationship of glucose and insulin levels to the risk of myocardial infarction: a case-control study  

Microsoft Academic Search

OBJECTIVETo assess the relationship between dysglycemia and myocardial infarction in nondiabetic individuals.BACKGROUNDNondiabetic hyperglycemia may be an important cardiac risk factor. The relationship between myocardial infarction and glucose, insulin, abdominal obesity, lipids and hypertension was therefore studied in South Asians—a group at high risk for coronary heart disease and diabetes.METHODSDemographics, waist\\/hip ratio, fasting blood glucose (FBG), insulin, lipids and glucose tolerance

Hertzel C Gerstein; Prem Pais; Janice Pogue; Salim Yusuf

1999-01-01

371

Resistant hypertension in the elderly-second line treatments: aldosterone antagonists, central alpha-agonist agents, alpha-adrenergic receptor blockers, direct vasodilators, and exogenous nitric oxide donors.  

PubMed

Resistant hypertension (RH) is a prevalent medical problem across all ages but is more frequent in elderly patients. This entity has to be distinguished from clinical settings which may simulate it such as apparent hypertension (pseudohypertension) or apparently resistant hypertension (pseudoresistant hypertension) [1]. An appropriate therapy for RH can be achieved by the addition of second line antihypertensive drugs: antialdosteronic diuretics, central agents, alpha blockers, direct vasodilating agents, and exogenous nitric oxide donors. These antihypertensive drugs are considered as second line drugs since they are less effective as monotherapy to reduce blood pressure (they induce counte regulatory responses that limit their antihypertensive effect such as volume expansion or reflex tachycardia) and prevent cardiovascular events, or due to significant adverse effects (postural hypotension, sedation, hyperkalemia). Second line drugs are also used when there is allergy or intolerance to the first line ones [2, 3]. PMID:25761104

Musso, Carlos G; Alfie, Jose

2015-01-01

372

Lactose malabsorption and intolerance: What should be the best clinical management?  

PubMed

Lactose malabsorption (LM) is the incomplete hydrolysis of lactose due to lactase deficiency, which may occur as a primary disorder or secondary to other intestinal diseases. Primary adult-type hypolactasia is an autosomal recessive condition resulting from the physiological decline of lactase activity. Different methods have been used to diagnose LM. Lactose breath test represents the most reliable technique. A recent consensus conference has proposed the more physiological dosage of 25 g of lactose and a standardized procedure for breath testing. Recently a new genetic test, based on C/T13910 polymorphism, has been proposed for the diagnosis of adult-type hypolactasia, complementing the role of breath testing. LM represents a well-known cause of abdominal symptoms although only some lactose malabsorbers are also intolerants. Diagnosing lactose intolerance is not straightforward. Many non-malabsorber subjects diagnose themselves as being lactose intolerant. Blind lactose challenge studies should be recommended to obtain objective results. Besides several studies indicate that subjects with lactose intolerance can ingest up to 15 g of lactose with no or minor symptoms. Therefore a therapeutic strategy consists of a lactose restricted diet avoiding the nutritional disadvantages of reduced calcium and vitamin intake.Various pharmacological options are also available. Unfortunately there is insufficient evidence that these therapies are effective. Further double-blind studies are needed to demonstrate treatment effectiveness in lactose intolerance. PMID:22966480

Usai-Satta, Paolo; Scarpa, Mariella; Oppia, Francesco; Cabras, Francesco

2012-06-01

373

Statin intolerance – an attempt at a unified definition. Position paper from an International Lipid Expert Panel  

PubMed Central

Statins are one of the most commonly prescribed drugs in clinical practice. They are usually well tolerated and effectively prevent cardiovascular events. Most adverse effects associated with statin therapy are muscle-related. The recent statement of the European Atherosclerosis Society (EAS) has focused on statin associated muscle symptoms (SAMS), and avoided the use of the term ‘statin intolerance’. Although muscle syndromes are the most common adverse effects observed after statin therapy, excluding other side effects might underestimate the number of patients with statin intolerance, which might be observed in 10–15% of patients. In clinical practice, statin intolerance limits effective treatment of patients at risk of, or with, cardiovascular disease. Knowledge of the most common adverse effects of statin therapy that might cause statin intolerance and the clear definition of this phenomenon is crucial to effectively treat patients with lipid disorders. Therefore, the aim of this position paper was to suggest a unified definition of statin intolerance, and to complement the recent EAS statement on SAMS, where the pathophysiology, diagnosis and the management were comprehensively presented.

Rizzo, Manfredi; Toth, Peter P.; Farnier, Michel; Davidson, Michael H.; Al-Rasadi, Khalid; Aronow, Wilbert S.; Athyros, Vasilis; Djuric, Dragan M.; Ezhov, Marat V.; Greenfield, Robert S.; Hovingh, G. Kees; Kostner, Karam; Serban, Corina; Lighezan, Daniel; Fras, Zlatko; Moriarty, Patrick M.; Muntner, Paul; Goudev, Assen; Ceska, Richard; Nicholls, Stephen J.; Broncel, Marlena; Nikolic, Dragana; Pella, Daniel; Puri, Raman; Rysz, Jacek; Wong, Nathan D.; Bajnok, Laszlo; Jones, Steven R.; Ray, Kausik K.; Mikhailidis, Dimitri P.

2015-01-01

374

Statin intolerance - an attempt at a unified definition. Position paper from an International Lipid Expert Panel.  

PubMed

Statins are one of the most commonly prescribed drugs in clinical practice. They are usually well tolerated and effectively prevent cardiovascular events. Most adverse effects associated with statin therapy are muscle-related. The recent statement of the European Atherosclerosis Society (EAS) has focused on statin associated muscle symptoms (SAMS), and avoided the use of the term 'statin intolerance'. Although muscle syndromes are the most common adverse effects observed after statin therapy, excluding other side effects might underestimate the number of patients with statin intolerance, which might be observed in 10-15% of patients. In clinical practice, statin intolerance limits effective treatment of patients at risk of, or with, cardiovascular disease. Knowledge of the most common adverse effects of statin therapy that might cause statin intolerance and the clear definition of this phenomenon is crucial to effectively treat patients with lipid disorders. Therefore, the aim of this position paper was to suggest a unified definition of statin intolerance, and to complement the recent EAS statement on SAMS, where the pathophysiology, diagnosis and the management were comprehensively presented. PMID:25861286

Banach, Maciej; Rizzo, Manfredi; Toth, Peter P; Farnier, Michel; Davidson, Michael H; Al-Rasadi, Khalid; Aronow, Wilbert S; Athyros, Vasilis; Djuric, Dragan M; Ezhov, Marat V; Greenfield, Robert S; Hovingh, G Kees; Kostner, Karam; Serban, Corina; Lighezan, Daniel; Fras, Zlatko; Moriarty, Patrick M; Muntner, Paul; Goudev, Assen; Ceska, Richard; Nicholls, Stephen J; Broncel, Marlena; Nikolic, Dragana; Pella, Daniel; Puri, Raman; Rysz, Jacek; Wong, Nathan D; Bajnok, Laszlo; Jones, Steven R; Ray, Kausik K; Mikhailidis, Dimitri P

2015-03-16

375

Genic Intolerance to Functional Variation and the Interpretation of Personal Genomes  

PubMed Central

A central challenge in interpreting personal genomes is determining which mutations most likely influence disease. Although progress has been made in scoring the functional impact of individual mutations, the characteristics of the genes in which those mutations are found remain largely unexplored. For example, genes known to carry few common functional variants in healthy individuals may be judged more likely to cause certain kinds of disease than genes known to carry many such variants. Until now, however, it has not been possible to develop a quantitative assessment of how well genes tolerate functional genetic variation on a genome-wide scale. Here we describe an effort that uses sequence data from 6503 whole exome sequences made available by the NHLBI Exome Sequencing Project (ESP). Specifically, we develop an intolerance scoring system that assesses whether genes have relatively more or less functional genetic variation than expected based on the apparently neutral variation found in the gene. To illustrate the utility of this intolerance score, we show that genes responsible for Mendelian diseases are significantly more intolerant to functional genetic variation than genes that do not cause any known disease, but with striking variation in intolerance among genes causing different classes of genetic disease. We conclude by showing that use of an intolerance ranking system can aid in interpreting personal genomes and identifying pathogenic mutations. PMID:23990802

Petrovski, Slavé; Wang, Quanli; Heinzen, Erin L.; Allen, Andrew S.; Goldstein, David B.

2013-01-01

376

Bone-specific insulin resistance disrupts whole-body glucose homeostasis via decreased osteocalcin activation.  

PubMed

Insulin signaling in osteoblasts has been shown recently to contribute to whole-body glucose homeostasis in animals fed a normal diet; however, it is unknown whether bone contributes to the insulin resistance that develops in animals challenged by a high-fat diet (HFD). Here, we evaluated the consequences of osteoblast-specific overexpression of or loss of insulin receptor in HFD-fed mice. We determined that the severity of glucose intolerance and insulin resistance that mice develop when fed a HFD is in part a consequence of osteoblast-dependent insulin resistance. Insulin resistance in osteoblasts led to a decrease in circulating levels of the active form of osteocalcin, thereby decreasing insulin sensitivity in skeletal muscle. Insulin resistance developed in osteoblasts as the result of increased levels of free saturated fatty acids, which promote insulin receptor ubiquitination and subsequent degradation. Together, these results underscore the involvement of bone, among other tissues, in the disruption of whole-body glucose homeostasis resulting from a HFD and the involvement of insulin and osteocalcin cross-talk in glucose intolerance. Furthermore, our data indicate that insulin resistance develops in bone as the result of lipotoxicity-associated loss of insulin receptors. PMID:24642469

Wei, Jianwen; Ferron, Mathieu; Clarke, Christopher J; Hannun, Yusuf A; Jiang, Hongfeng; Blaner, William S; Karsenty, Gerard

2014-04-01

377

Myocardial remodeling in hypertension.  

PubMed

Left ventricular (LV) hypertrophy and remodeling are frequently seen in hypertensive subjects and result from a complex interaction of several hemodynamic and non-hemodynamic variables. Although increased blood pressure is considered the major determinant of LV structural alterations, ethnicity, gender, environmental factors, such as salt intake, obesity and diabetes mellitus, as well as neurohumoral and genetic factors might influence LV mass and geometry. The conventional concept of hypertensive LV remodeling has been that hypertension leads to concentric hypertrophy, as an adaptive response to normalize wall stress, which is then followed by chamber dilation and heart failure. However, several lines of evidence have challenged this dogma. Concentric hypertrophy is not the most frequent geometric pattern and is less usually seen than eccentric hypertrophy in hypertensive subjects. In addition, data from recent studies suggested that transition from LV concentric hypertrophy to dilation and systolic dysfunction is not a common finding, especially in the absence of coronary heart disease. LV hypertrophy is also consistently associated with increased cardiovascular morbidity and mortality, raising doubts whether this phenotype is an adaptive response. Experimental evidence exists that a blunting of load-induced cardiomyocyte hypertrophy does not necessarily result in LV dysfunction or failure. Furthermore, the hypertrophic myocardium shows fibrosis, alterations in the coronary circulation and cardiomyocyte apoptosis, which may result in heart failure, myocardial ischemia and arrhythmias. Overall, this body of evidence suggests that LV hypertrophy is a complex phenotype that predicts adverse cardiovascular outcomes and may not be necessarily considered as an adaptive response to systemic hypertension. PMID:24804791

Nadruz, W

2015-01-01

378

Pregnancy with portal hypertension.  

PubMed

Even though pregnancy is rare with cirrhosis and advanced liver disease, but it may co-exist in the setting of non-cirrhotic portal hypertension as liver function is preserved but whenever encountered together is a complex clinical dilemma. Pregnancy in a patient with portal hypertension presents a special challenge to the obstetrician as so-called physiological hemodynamic changes associated with pregnancy, needed for meeting demands of the growing fetus, worsen the portal hypertension thereby putting mother at risk of potentially life-threatening complications like variceal hemorrhage. Risks of variceal bleed and hepatic decompensation increase many fold during pregnancy. Optimal management revolves round managing the portal hypertension and its complications. Thus management of such cases requires multi-speciality approach involving obstetricians experienced in dealing with high risk cases, hepatologists, anesthetists and neonatologists. With advancement in medical field, pregnancy is not contra-indicated in these women, as was previously believed. This article focuses on the different aspects of pregnancy with portal hypertension with special emphasis on specific cause wise treatment options to decrease the variceal bleed and hepatic decompensation. Based on extensive review of literature, management from pre-conceptional period to postpartum is outlined in order to have optimal maternal and perinatal outcomes. PMID:25755552

Aggarwal, Neelam; Negi, Neha; Aggarwal, Aakash; Bodh, Vijay; Dhiman, Radha K

2014-06-01

379

Pregnancy with Portal Hypertension  

PubMed Central

Even though pregnancy is rare with cirrhosis and advanced liver disease, but it may co-exist in the setting of non-cirrhotic portal hypertension as liver function is preserved but whenever encountered together is a complex clinical dilemma. Pregnancy in a patient with portal hypertension presents a special challenge to the obstetrician as so-called physiological hemodynamic changes associated with pregnancy, needed for meeting demands of the growing fetus, worsen the portal hypertension thereby putting mother at risk of potentially life-threatening complications like variceal hemorrhage. Risks of variceal bleed and hepatic decompensation increase many fold during pregnancy. Optimal management revolves round managing the portal hypertension and its complications. Thus management of such cases requires multi-speciality approach involving obstetricians experienced in dealing with high risk cases, hepatologists, anesthetists and neonatologists. With advancement in medical field, pregnancy is not contra-indicated in these women, as was previously believed. This article focuses on the different aspects of pregnancy with portal hypertension with special emphasis on specific cause wise treatment options to decrease the variceal bleed and hepatic decompensation. Based on extensive review of literature, management from pre-conceptional period to postpartum is outlined in order to have optimal maternal and perinatal outcomes. PMID:25755552

Aggarwal, Neelam; Negi, Neha; Aggarwal, Aakash; Bodh, Vijay; Dhiman, Radha K.

2014-01-01

380

Association of glucose transporter 4 genetic Polymorphisms with obstructive sleep apnea syndrome in Han Chinese general population: a cross-section study  

PubMed Central

Background Obstructive sleep apnea syndrome (OSAS) is strongly associated with the increasing prevalence of cerebrovascular events and metabolic syndrome. A growing number of studies have shown OSAS is an independent factor for insulin resistance, glucose intolerance and type2 diabetes. However, relationship of OSAS with dysglycemia is complex and still remains poorly understood. Glucose transporter 4 (GLUT4) gene is Human and rodents’ main glucose transporter sensitive to insulin, and therefore confirmation of candidate gene polymorphisms and association with OSAS is needed. Aim of our study was to assess whether GLUT4 gene polymorphisms are associated with OSAS. Methods Patients hospitalized at People’s Hospital of Xinjiang were selected from January to December 2010. A total of 568 Han subjects who possibly exist OSAS base on a history and physical examination were completed the polysomnography, 412of whom (72.5%) were diagnosed with OSAS, and 156 individuals were confirmed without OSAS (27.5%). 96 severe OSAS patients chosen from OSAS were used for DNA sequencing in functional domain. Blood samples were collected from all subjects and genotyping was performed on DNA extracted from blood cells. Results We performed GLUT4 genome sequencing, found 4 mutated sites. And finally selected three mutated sites such as rs5415, rs4517 and rs5435, according to principle of linkage disequilibrium (r 2 > 0.8) and minimum gene allele frequency > 5%. All SNPs satisfied HEW (P > 0.05). Our study demonstrated a significant association of GLUT4 SNPrs5417 allele with OSAS, compared with controls (P < 0.05). Haplotype H1 (TCC) and H3 (CCC) defined as SNPrs5415, rs4517 and rs5435 are marginally associated with OSAS (P < 0.05). Frequencies of C haplotype of rs5417 in OSAS were higher than in controls. After adjustment for confounding factors, (AC + AA) genotype significantly reduces prevalence of OSAS, compared with CC genotype. Level of awake blood oxygen and lowest blood oxygen of (AA + AC) genotype was significantly superior to those of CC genotype. Conclusions Our study demonstrates GLUT4 gene SNPrs5417 is associated with OSAS in hypertensive population. Carriers of AA + AC have less prevalence of obstructive sleep apnea syndrome than that of CC carriers. PMID:24410986

2014-01-01

381

Blood pressure and plasma renin activity as predictors of orthostatic intolerance  

NASA Technical Reports Server (NTRS)

The effect of 3 h standing, followed by a period of head-up tilt (HUT) on physiological response (orthostatic tolerance, blood pressure and heart rate), as well as on plasma vasopressin (PVP) and renin activity (PRA) were studied in 13 dehydrated (to 2.4 pct loss of body weight) subjects. Seven subjects showed signs of orthostatic intolerance (INT), manifested by sweating, pallor, nausea and dizziness. Prior to these symptoms, the INT subjects exhibited lower systolic (SP) and pulse (PP) pressures, and an elevated PRA, compared to the tolerant (TOL) subjects. HUT has aggravated increases of RPA in the INT subjects and caused an increase, higher than in TOL subjects, in PVP, while rehydration has greatly attenuated the PVP response to the HUT and decreased the PRA response. It is concluded that dehydration, together with measurements of SP, PP and PRA, may serve as a means of predicting orthostatic intolerance and may provide a physiological model for studying the causes of intolerance.

Harrison, M. H.; Kravik, S. E.; Geelen, G.; Keil, L.; Greenleaf, J. E.

1985-01-01

382

Odor and Noise Intolerance in Persons with Self-Reported Electromagnetic Hypersensitivity  

PubMed Central

Lack of confirmation of symptoms attributed to electromagnetic fields (EMF) and triggered by EMF exposure has highlighted the role of individual factors. Prior observations indicate intolerance to other types of environmental exposures among persons with electromagnetic hypersensitivity (EHS). This study assessed differences in odor and noise intolerance between persons with EHS and healthy controls by use of subscales and global measures of the Chemical Sensitivity Scale (CSS) and the Noise Sensitivity Scale (NSS). The EHS group scored significantly higher than the controls on all CSS and NSS scales. Correlation coefficients between CSS and NSS scores ranged from 0.60 to 0.65 across measures. The findings suggest an association between EHS and odor and noise intolerance, encouraging further investigation of individual factors for understanding EMF-related symptoms. PMID:25166918

Nordin, Steven; Neely, Gregory; Olsson, David; Sandström, Monica

2014-01-01

383

Orthostatic intolerance and the postural tachycardia syndrome: genetic and environment pathophysiologies. Neurolab Autonomic Team  

NASA Technical Reports Server (NTRS)

Orthostatic intolerance is a common problem for inbound space travelers. There is usually tachycardia on standing but blood pressure may be normal, low or, rarely, elevated. This condition is analogous to the orthostatic intolerance that occurs on Earth in individuals with orthostatic tachycardia, palpitations, mitral valve prolapse, and light-headedness. Our studies during the Neurolab mission indicated that sympathetic nerve traffic is raised in microgravity and that plasma norepinephrine is higher than baseline supine levels but lower than baseline upright levels. A subgroup of patients with familial orthostatic intolerance differ from inbound space travelers in that they have an alanine-to-to-proline mutation at amino acid position 457 in their norepinephrine transporter gene. This leads to poor clearance of norepinephrine from synapses, with consequent raised heart rate. Clinical features of these syndromes are presented.

Robertson, D.; Shannon, J. R.; Biaggioni, I.; Ertl, A. C.; Diedrich, A.; Carson, R.; Furlan, R.; Jacob, G.; Jordan, J.

2000-01-01

384

Functional sympatholysis in hypertension.  

PubMed

Sympathetic vasoconstriction is normally attenuated in exercising muscle by local changes in muscle metabolites and other substances that reduce vascular responsiveness to ?-adrenergic receptor activation. Termed functional sympatholysis, this protective mechanism is thought to optimize muscle blood flow distribution to match perfusion with metabolic demand. Emerging evidence from both animal and human studies indicate that functional sympatholysis is impaired in hypertension and may constitute an important underlying cause of skeletal muscle malperfusion during exercise in this common cardiovascular condition. Findings from studies of animal models of hypertension and patients with essential hypertension will be integrated in this review to provide insight into the underlying mechanisms responsible for inappropriate sympathetic vasoconstriction in exercising muscle and the treatment options that may restore functional sympatholysis and improve muscle perfusion during exercise. PMID:25458424

Thomas, Gail D

2015-03-01

385

The Dietary Approaches to Stop Hypertension (DASH) Eating Pattern in Special Populations  

PubMed Central

The Dietary Approaches to Stop Hypertension (DASH) trial showed that a diet rich in fruits, vegetables, low-fat dairy products with reduced total and saturated fat, cholesterol, and sugar-sweetened products effectively lowers blood pressure in individuals with prehypertension and stage I hypertension. Limited evidence is available on the safety and efficacy of the DASH eating pattern in special patient populations that were excluded from the trial. Caution should be exercised before initiating the DASH diet in patients with chronic kidney disease, chronic liver disease, and those who are prescribed renin-angiotensin-aldosterone system antagonist, but these conditions are not strict contraindications to DASH. Modifications to the DASH diet may be necessary to facilitate its use in patients with chronic heart failure, uncontrolled diabetes mellitus type II, lactose intolerance, and celiac disease. In general, the DASH diet can be adopted by most patient populations and initiated simultaneously with medication therapy and other lifestyle interventions. PMID:22846984

Tyson, Crystal C.; Nwankwo, Chinazo; Lin, Pao-Hwa; Svetkey, Laura P.

2015-01-01

386

Oxidative stress and hypertension.  

PubMed

This review has summarized some of the data supporting a role of ROS and oxidant stress in the genesis of hypertension. There is evidence that hypertensive stimuli, such as high salt and angiotensin II, promote the production of ROS in the brain, the kidney, and the vasculature and that each of these sites contributes either to hypertension or to the untoward sequelae of this disease. Although the NADPH oxidase in these various organs is a predominant source, other enzymes likely contribute to ROS production and signaling in these tissues. A major clinical challenge is that the routinely used antioxidants are ineffective in preventing or treating cardiovascular disease and hypertension. This is likely because these drugs are either ineffective or act in a non-targeted fashion, such that they remove not only injurious ROS Fig. 5. Proposed role of T cells in the genesis of hypertension and the role of the NADPH oxidase in multiple cells/organs in modulating this effect. In this scenario, angiotensin II stimulates an NADPH oxidase in the CVOs of the brain, increasing sympathetic outflow. Sympathetic nerve terminals in lymph nodes activate T cells, and angiotensin II also directly activates T cells. These stimuli also activate expression of homing signals in the vessel and likely the kidney, which attract T cells to these organs. T cells release cytokines that stimulate the vessel and kidney NADPH oxidases, promoting vasoconstriction and sodium retention. SFO, subfornical organ. 630 Harrison & Gongora but also those involved in normal cell signaling. A potentially important and relatively new direction is the concept that inflammatory cells such as T cells contribute to hypertension. Future studies are needed to understand the interaction of T cells with the CNS, the kidney, and the vasculature and how this might be interrupted to provide therapeutic benefit. PMID:19427495

Harrison, David G; Gongora, Maria Carolina

2009-05-01

387

Hypertension in terminal renal failure  

Microsoft Academic Search

Hypertension in terminal renal failure. Inverse interrelations between plasma renin activity and exchangeable sodium or blood volume were found in both normotensive (N = 23) and hypertensive (N = 29) hemodialysis patients (r = 0.47; P < 0.005); however, mean plasma renin for any given sodium\\/volume state was at least two-fold higher in hypertensive than in normotensive hemodialysis patients or

Peter Weidmann; Carlo Beretta-Piccoli; Fritz Steffen; Alfred Blumberg; François C Reubi

1976-01-01

388

TREATMENT OF THE METABOLIC SYNDROME: THE IMPACT OF LIFESTYLE MODIFICATION  

Technology Transfer Automated Retrieval System (TEKTRAN)

Along with the increasing prevalence of obesity comes a constellation of metabolic derangements: dyslipidemias, hypertension, insulin resistance, and glucose intolerance, as well as increased prothrombotic and inflammatory markers. The association of these factors has been termed the "metabolic synd...

389

QUANTITATIVE GENETIC ANALYSIS OF THE METABOLIC SYNDROME IN HISPANIC CHILDREN  

Technology Transfer Automated Retrieval System (TEKTRAN)

Childhood obesity is associated with a constellation of metabolic derangements including glucose intolerance, hypertension, and dyslipidemia, referred to as the metabolic syndrome. The purpose of this study was to investigate genetic and environmental factors contributing to the metabolic syndrome i...

390

Glucose-Insulin  

NSDL National Science Digital Library

Glucose is the vehicle by which energy gets from digested food to the cells of the body. In Type I diabetes mellitus, insufficient insulin is available to help get glucose out of the blood and into the cells of the body. This activity has been designed so that students can investigate the negative feedback loop between blood glucose and insulin, one of the mechanisms designed to maintain homeostasis in the human body.

Maryland Virtual High School

391

The glucose oxidase-peroxidase assay for glucose  

Technology Transfer Automated Retrieval System (TEKTRAN)

The glucose oxidase-peroxidase assay for glucose has served as a very specific, sensitive, and repeatable assay for detection of glucose in biological samples. It has been used successfully for analysis of glucose in samples from blood and urine, to analysis of glucose released from starch or glycog...

392

Contact lens intolerance: refitting with dual axis lens for corneal refractive therapy  

PubMed Central

Corneal refractive therapy is a non-surgical procedure whose main purpose is to improve uncorrected visual acuity during the day, without spectacles or contact lenses. We report an adult woman who shows contact lens intolerance and does not want to wear eyeglasses. We used dual axis contact lens to improve lens centration. We demonstrate a maintained unaided visual acuity during one year of treatment. In conclusion, we can consider refitting with dual axis lens for corneal refractive therapy as a non-surgical option for patients who show contact lens intolerance.

López-López, María; Pelegrín-Sánchez, José Miguel; Sobrado-Calvo, Paloma; García-Ayuso, Diego

2011-01-01

393

Hyperglycemia (High Blood Glucose)  

MedlinePLUS

... Complications Neuropathy Foot Complications DKA (Ketoacidosis) & Ketones Kidney Disease (Nephropathy) Gastroparesis Mental Health Treatment & Care Blood Glucose Testing Medication Doctors, Nurses & More ...

394

All about Blood Glucose  

MedlinePLUS

... usingthe resultsfromyourdailybloodglucosetestingandyour A1Ccheck. What makes my blood glucose levels rise or fall? Bloodglucoselevelsriseandfallthroughoutthe day. Onekeytotakingcareofyourdiabetesis understanding whyitrisesandfalls.Ifyouknow ...

395

Tolerability of long term therapy with enalapril maleate in patients resistant to other therapies and intolerant to captopril.  

PubMed

Patients with severe hypertension and/or congestive heart failure (n = 281) who were unresponsive to other therapies and intolerant to captopril received enalapril treatment (mean dose 19.5 mg/day) under study conditions as part of a Compassionate Use Program. Many of these patients had serious concurrent disorders known to predispose them to a greater risk of adverse experiences and death. The mean duration of enalapril treatment was 29 weeks, with a range of 1 day to approximately 3.5 years. Enalapril was generally well tolerated, and the estimated long term probability of patients terminating enalapril therapy because of adverse effects was low. 20 patients had discontinued captopril treatment because of low white blood cell counts; during subsequent enalapril treatment these reactions resolved in 14 patients, persisted in 2 patients, and could not be evaluated in 4 patients. Captopril-related proteinuria improved or resolved in 9 and persisted in 2 of 15 patients, taste disturbances resolved in 35 and persisted in 2 of 38 patients; and rash resolved in all but 7 of 178 patients during enalapril treatment. 18 patients (6%) discontinued enalapril treatment because of lack of efficacy; 6 of these 18 patients died due to a progression of heart failure, and another 11 patients died for other reasons. The deaths were considered unrelated to therapy with enalapril. Adverse reactions were the reason for discontinuation of enalapril treatment in 53 patients (19%). The most common adverse experiences that resulted in discontinuation of enalapril were: impairment of renal function (5%), hypotension (2%) and rash (2%). No neutropenia, proteinuria, or new taste disturbances were recorded as reasons for discontinuation.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:2541310

Rucinska, E J; Small, R; Mulcahy, W S; Snyder, D L; Rodel, P V; Rush, J E; Smith, R D; Walker, J F; Irvin, J D

1989-01-01

396

Oxidative stress and hypertension: Possibility of hypertension therapy with antioxidants  

PubMed Central

Hypertension is a major risk factor for myocardial infarction, heart failure, stroke, peripheral arterial disease, and aortic aneurysm, and is a cause of chronic kidney disease. Hypertension is often associated with metabolic abnormalities such as diabetes and dyslipidemia, and the rate of these diseases is increasing nowadays. Recently it has been hypothesized that oxidative stress is a key player in the pathogenesis of hypertension. A reduction in superoxide dismutase and glutathione peroxidase activity has been observed in newly diagnosed and untreated hypertensive subjects, which are inversely correlated with blood pressure. Hydrogen peroxide production is also higher in hypertensive subjects. Furthermore, hypertensive patients have higher lipid hydroperoxide production. Oxidative stress is also markedly increased in hypertensive patients with renovascular disease. If oxidative stress is indeed a cause of hypertension, then, antioxidants should have beneficial effects on hypertension control and reduction of oxidative damage should result in a reduction in blood pressure. Although dietary antioxidants may have beneficial effects on hypertension and cardiovascular risk factors, however, antioxidant supplementation has not been shown consistently to be effective and improvement is not usually seen in blood pressure after treatment with single or combination antioxidant therapy in subjects thought to be at high risk of cardiovascular disease. This matter is the main focus of this paper. A list of medicinal plants that have been reported to be effective in hypertension is also presented. PMID:25097610

Baradaran, Azar; Nasri, Hamid; Rafieian-Kopaei, Mahmoud

2014-01-01

397

Pulmonary hypertension caused by pulmonary venous hypertension  

PubMed Central

Abstract The effect of pulmonary venous hypertension (PVH) on the pulmonary circulation is extraordinarily variable, ranging from no impact on pulmonary vascular resistance (PVR) to a marked increase. The reasons for this are unknown. Both acutely reversible pulmonary vasoconstriction and pathological remodeling (especially medial hypertrophy and intimal hyperplasia) account for increased PVR when present. The mechanisms involved in vasoconstriction and remodeling are not clearly defined, but increased wall stress, especially in small pulmonary arteries, presumably plays an important role. Myogenic contraction may account for increased vascular tone and also indirectly stimulate remodeling of the vessel wall. Increased wall stress may also directly cause smooth muscle growth, migration, and intimal hyperplasia. Even long-standing and severe pulmonary hypertension (PH) usually abates with elimination of PVH, but PVH-PH is an important clinical problem, especially because PVH due to left ventricular noncompliance lacks definitive therapy. The role of targeted PH therapy in patients with PVH-PH is unclear at this time. Most prospective studies indicate that these medications are not helpful or worse, but there is ample reason to think that a subset of patients with PVH-PH may benefit from phosphodiesterase inhibitors or other agents. A different approach to evaluating possible pharmacologic therapy for PVH-PH may be required to better define its possible utility. PMID:25610595

2014-01-01

398

Young and old genetically heterogeneous HET3 mice on a rapamycin diet are glucose intolerant but insulin sensitive  

E-print Network

Rapamycin, an inhibitor of the mechanistic target of rapamycin (mTOR) signaling pathway, extends the life span of yeast, worms, flies, and mice. Interventions that promote longevity are often correlated with increased ...

Lamming, Dudley W.

399

High-fat hypercaloric diet induces obesity, glucose intolerance and hyperlipidemia in normal adult male Wistar rat  

Microsoft Academic Search

There is strong evidence that genetic factors contribute to the development of obesity in humans as well as laboratory animals. Another important factor leading to obesity is an increase in energy intake. However, it is difficult to make normal rats obese by controlling daily food intake. There is no report of normal adult male Wistar rats becoming obese and diabetic

Toshiharu Akiyama; Issei Tachibana; Hisashi Shirohara; Nobuaki Watanabe; Makoto Otsuki

1996-01-01

400

Synergistic effects of genetic beta cell dysfunction and maternal glucose intolerance on offspring metabolic phenotype in mice  

Microsoft Academic Search

Aims\\/hypothesis  Diabetes in pregnancy is linked to development of obesity in the offspring, but the mechanisms are not fully understood. Gestational\\u000a diabetes mellitus (GDM) occurs when beta cells are unable to compensate for the normal insulin resistance of late pregnancy.\\u000a In this study, we used a murine model of beta cell dysfunction to examine the effects of maternal GDM on phenotype

S. M. Lau; S. Lin; R. A. Stokes; K. Cheng; P. A. Baldock; R. F. Enriquez; M. McLean; N. W. Cheung; A. Sainsbury; F. J. Gonzalez; H. Herzog; J. E. Gunton

2011-01-01

401

Orthostatic intolerance predicts mild cognitive impairment: incidence of mild cognitive impairment and dementia from the Swedish general population cohort Good Aging in Skåne  

PubMed Central

Introduction Contradictory results have been reported on the relationship between orthostatic hypotension (OH) and mild cognitive impairment (MCI). Objective To study the incidence of MCI and dementia and their relationship to OH and subclinical OH with orthostatic symptoms (orthostatic intolerance). Study design and setting This study used a prospective general population cohort design and was based on data from the Swedish Good Aging in Skåne study (GÅS-SNAC), they were studied 6 years after baseline of the present study, with the same study protocol at baseline and at follow-up. The study sample comprised 1,480 randomly invited subjects aged 60 to 93 years, and had a participation rate of 82% at follow-up. OH test included assessment of blood pressure and symptoms of OH. Results The 6-year incidence of MCI was 8%, increasing from 12.1 to 40.5 per 1,000 person-years for men and 6.9 to 16.9 per 1,000 person-years for women aged 60 to >80 years. The corresponding 6-year incidence of dementia was 8%. Orthostatic intolerance during uprising was related to risk for MCI at follow-up (odds ratio [OR] =1.84 [1.20–2.80][95% CI]), adjusted for age and education independently of blood pressure during testing. After stratification for hypertension (HT), the corresponding age-adjusted OR for MCI in the non-HT group was 1.71 (1.10–2.31) and 1.76 (1.11–2.13) in the HT group. Among controls, the proportion of those with OH was 16%; those with MCI 24%; and those with dementia 31% (age-adjusted OR 1.93 [1.19–3.14]). Conclusion Not only OH, but also symptoms of OH, seem to be a risk factor for cognitive decline and should be considered in the management of blood pressure among the elderly population. PMID:25429211

Elmståhl, Sölve; Widerström, Elisabet

2014-01-01

402

“Renovascular Hypertension: Is there still a role for stent revascularization? ” Current Opinion in Nephrology and Hypertension  

PubMed Central

Purpose Management of renovascular hypertension remains controversial and problematic, in part due to failure of prospective trials to demonstrate added benefit to revascularization. Recent Findings Effective drug therapy often can achieve satisfactory blood pressure control, although concerns persist for the potential for progressive, delayed loss of kidney function beyond a stenotic lesion. Recent studies highlight benefits of renal artery stenting in subsets of patients including those with recurrent pulmonary edema and those intolerant to blockade of the renin-angiotensin system. Occasional patients with recent deterioration in renal function recover sufficient GFR after stenting to avoid requirements for renal replacement therapy. Emerging paradigms from both clinical and experimental studies suggest that hypoxic injury within the kidney activates inflammatory injury pathways and microvascular rarification that may not recover after technically successful revascularization alone. Initial data suggest that additional measures to repair the kidney, including the use of cell-based therapy, may offer the potential to recover kidney function in advanced renovascular disease. Summary Specific patient groups benefit from renal revascularization. Nephrologists will increasingly be asked to manage complex renovascular patients different from those in randomized trials that require intensely individualized management. PMID:23917028

Textor, Stephen C.

2014-01-01

403

Acute Melatonin Administration in Humans Impairs Glucose Tolerance in Both the Morning and Evening  

PubMed Central

Study Objectives: To study the effect of melatonin administration on glucose metabolism in humans in the morning and evening. Design: Placebo-controlled, single-blind design. Setting: Laboratory assessments. Participants: 21 healthy women (24 ± 6 y; body mass index: 23.0 ± 3.3 kg/m2). Interventions: Glucose tolerance was assessed by oral glucose tolerance tests (OGTT; 75 g glucose) on 4 occasions: in the morning (9 AM), and evening (9 PM); each occurring 15 minutes after melatonin (5 mg) and placebo administration on 4 non-consecutive days. Measurements and Results: Melatonin administration impaired glucose tolerance. When administered in the morning, melatonin significantly increased the incremental area under the curve (AUC) and maximum concentration (Cmax) of plasma glucose following OGTT by 186% and 21%, respectively, as compared to placebo; while in the evening, melatonin significantly increased glucose AUC and Cmax by 54% and 27%, respectively. The effect of melatonin on the insulin response to the OGTT depended on the time of day (P < 0.05). In the morning, melatonin decreased glucose tolerance primarily by decreasing insulin release, while in the evening, by decreasing insulin sensitivity. Conclusions: Acute melatonin administration in humans impairs glucose tolerance in both the morning and evening. When administering melatonin, the proximity to meal timing may need to be considered, particularly in those at risk for glucose intolerance. Citation: Rubio-Sastre P, Scheer FA, Gómez-Abellán P, Madrid JA, Garaulet M. Acute melatonin administration in humans impairs glucose tolerance in both the morning and evening. SLEEP 2014;37(10):1715-1719. PMID:25197811

Rubio-Sastre, Patricia; Scheer, Frank A.J.L.; Gómez-Abellán, Purificación; Madrid, Juan A.; Garaulet, Marta

2014-01-01

404

The prevalence of glucose metabolism abnormalities in Greek women with polycystic ovary syndrome.  

PubMed

The prevalence of glucose metabolism abnormalities in PCOS women worldwide varies between 10 and 40% but there are no data in Greek PCOS women. In this retrospective study the prevalence of glucose abnormalities and the indices of insulin resistance (IR) and whole-body insulin sensitivity were estimated in a Greek population with PCOS. Impaired glucose tolerance (IGT), impaired fasting glucose (IFG) and type 2 diabetes mellitus (t2DM) were calculated. The prevalence of IGT, IFG and t2DM in our PCOS population was 7.6, 5.1 and 1.7%, respectively. The total prevalence of glucose abnormalities was estimated as 14.1%. The prevalence of t2DM was three- to four-fold higher than in the general Greek female population of the same age as this was estimated by 2, recently published studies. PCOS women with increased BMI and waist circumference and age greater than 30 years, present more severe IR and decreased whole-body insulin sensitivity. Our data indicates a relatively high prevalence of glucose intolerance and t2DM in a Greek population with PCOS. Obese women with PCOS are in higher risk to develop glucose abnormalities and probably t2DM later in life and therefore every woman diagnosed with PCOS should undergo a 2-h post load OGTT. PMID:22571176

Trakakis, Eftihios; Basios, George; Peppa, Melpomeni; Simeonidis, George; Labos, George; Creatsa, Maria; Misailidou, Maria; Boutati, Eleni; Vaggopoulos, Vassilios; Panagopoulos, Perikles; Dimitriades, George; Kassanos, Dimitrios

2012-11-01

405

Idiopathic pulmonary arterial hypertension.  

PubMed

Idiopathic pulmonary arterial hypertension (IPAH), formerly called primary pulmonary hypertension, is a rare disease (incidence and prevalence rates of approximately one and six cases per million inhabitants, respectively) with different clinical phenotypes. A group of diverse conditions manifest pulmonary arterial hypertension (PAH) and share similar pathological and/or clinical findings with IPAH. By definition, IPAH is diagnosed only after alternative diagnoses have been ruled out. Extensive investigation is needed to determine if PAH is associated with thyroid diseases, infectious diseases, autoimmune conditions, exposure to certain drugs (particularly anorexigens), certain genetic mutations, and so on. The presence of genetic abnormalities and risk factors (such as specific drug exposures) reinforces the "multiple hit" concept for the development of pulmonary hypertension. Fortunately, within the past two decades, therapeutic options have become available for IPAH, resulting in improved survival and clinical outcomes. At least seven different compounds have been registered for PAH treatment. However, even with aggressive PAH-specific therapy, mortality rates remain high (?40% at 5 years). Given the high mortality rates, the use of combinations of agents that work by different pathways has been advocated (either as "add-on" therapy or initial "up front" therapy). Further, new therapeutic agents and treatment strategies are on the near horizon, aiming to further improve survival from the remarkable progress already seen. PMID:24037625

Souza, Rogerio; Jardim, Carlos; Humbert, Marc

2013-10-01

406

Aldosterone and arterial hypertension  

Microsoft Academic Search

In the setting of primary aldosteronism, elevated aldosterone levels are associated with increased blood pressure. Aldosterone concentrations within the normal range, however, can also alter blood pressure. Furthermore, the aldosterone-to-renin ratio, an indicator of aldosterone excess, is associated with hypertension, even in patients without excessive absolute aldosterone levels. In this Review we assess the data on the role of aldosterone

Stefan Pilz; Eberhard Ritz; Barbara Obermayer-Pietsch; Thomas R. Pieber; Andreas Tomaschitz

2009-01-01

407

[Hypertension and sports activity].  

PubMed

The importance of physical activity in primary and secondary prevention of cardiovascular disease has been demonstrated in many studies. In particular, the effect of exercise, especially aerobioc exercise, is to reduce blood pressure and heart rate by reducing sympathetic tone, and to correct many factors of the metabolic syndrome. Exercise prescription should be based on knowledge of the changes induced by training, but also on risk assessment, both cardiovascular and non-cardiovascular, of hypertensive subjects. It is generally accepted that for prevention and treatment of hypertension is useful to perform 3-4 weekly sessions of aerobic exercise for 30-45 min, at 50-70% of maximum working capacity. The recommended activities are walking, running, cycling and programs of mixed aerobic exercise. People with hypertension may follow their own personal inclinations, by choosing a sport and doing it at a competitive level. In hypertensive athletes the eligibility for competitive sports activities implies a careful medical evaluation, according to the recently published Italian COCIS cardiac guidelines. PMID:21416836

Mos, Lucio; Driussi, Caterina; Mihaleje, Martina

2010-10-01

408

Sleep Apnea and Hypertension  

Microsoft Academic Search

\\u000a Sleep disordered breathing (SDB) encompasses all forms of respiratory disorders specific to sleep (1). There is a spectrum of SDB ranging from mild to severe with the most severe form being obstructive sleep apnea (OSA) (2). In adults, OSA has been linked to cardiovascular disease, specifically hypertension (HTN) (3). The association between systemic HTN and OSA is well documented in

Alisa A. Acosta

409

Paranormal healing and hypertension  

Microsoft Academic Search

A prospective randomised trial was carried out to see whether paranormal healing by laying on of hands might reduce blood pressure in essential hypertension and whether such an effect might be due to a paranormal, psychological, or placebo factor. Patients were randomised to three treatment groups: paranormal healing by laying on of hands (n=40), paranormal healing at a distance (n=37),

Jaap J Beutler; Johannes T M Attevelt; Sybo A Schouten; Joop A J Faber; Evert J Dorhout Mees; Gijsbert G Geijskes

1988-01-01

410

Redox signaling in hypertension  

Microsoft Academic Search

Diseases such as hypertension, atherosclerosis and diabetes are associated with vascular functional and structural changes including endothelial dysfunction, altered contractility and vascular remodeling. Cellular events underlying these processes involve changes in vascular smooth muscle cell (VSMC) growth, apoptosis\\/anoikis, cell migration, inflammation, and fibrosis. Many stimuli influence cellular changes, including mechanical forces, such as shear stress, and vasoactive agents, of which

Tamara M. Paravicini; Rhian M. Touyz

2006-01-01

411

GLUT2, glucose sensing and glucose homeostasis.  

PubMed

The glucose transporter isoform GLUT2 is expressed in liver, intestine, kidney and pancreatic islet beta cells, as well as in the central nervous system, in neurons, astrocytes and tanycytes. Physiological studies of genetically modified mice have revealed a role for GLUT2 in several regulatory mechanisms. In pancreatic beta cells, GLUT2 is required for glucose-stimulated insulin secretion. In hepatocytes, suppression of GLUT2 expression revealed the existence of an unsuspected glucose output pathway that may depend on a membrane traffic-dependent mechanism. GLUT2 expression is nevertheless required for the physiological control of glucose-sensitive genes, and its inactivation in the liver leads to impaired glucose-stimulated insulin secretion, revealing a liver-beta cell axis, which is likely to be dependent on bile acids controlling beta cell secretion capacity. In the nervous system, GLUT2-dependent glucose sensing controls feeding, thermoregulation and pancreatic islet cell mass and function, as well as sympathetic and parasympathetic activities. Electrophysiological and optogenetic techniques established that Glut2 (also known as Slc2a2)-expressing neurons of the nucleus tractus solitarius can be activated by hypoglycaemia to stimulate glucagon secretion. In humans, inactivating mutations in GLUT2 cause Fanconi-Bickel syndrome, which is characterised by hepatomegaly and kidney disease; defects in insulin secretion are rare in adult patients, but GLUT2 mutations cause transient neonatal diabetes. Genome-wide association studies have reported that GLUT2 variants increase the risks of fasting hyperglycaemia, transition to type 2 diabetes, hypercholesterolaemia and cardiovascular diseases. Individuals with a missense mutation in GLUT2 show preference for sugar-containing foods. We will discuss how studies in mice help interpret the role of GLUT2 in human physiology. PMID:25421524

Thorens, Bernard

2015-02-01

412

Inhibition of pancreatic ?-cell Ca2+/calmodulin-dependent protein kinase II reduces glucose-stimulated calcium influx and insulin secretion, impairing glucose tolerance.  

PubMed

Glucose-stimulated insulin secretion (GSIS) from pancreatic ?-cells is caused by Ca(2+) entry via voltage-dependent Ca(2+) channels. CaMKII is a key mediator and feedback regulator of Ca(2+) signaling in many tissues, but its role in ?-cells is poorly understood, especially in vivo. Here, we report that mice with conditional inhibition of CaMKII in ?-cells show significantly impaired glucose tolerance due to decreased GSIS. Moreover, ?-cell CaMKII inhibition dramatically exacerbates glucose intolerance following exposure to a high fat diet. The impairment of islet GSIS by ?-cell CaMKII inhibition is not accompanied by changes in either glucose metabolism or the activities of KATP and voltage-gated potassium channels. However, glucose-stimulated Ca(2+) entry via voltage-dependent Ca(2+) channels is reduced in islet ?-cells with CaMKII inhibition, as well as in primary wild-type ?-cells treated with a peptide inhibitor of CaMKII. The levels of basal ?-cell cytoplasmic Ca(2+) and of endoplasmic reticulum Ca(2+) stores are also decreased by CaMKII inhibition. In addition, CaMKII inhibition suppresses glucose-stimulated action potential firing frequency. These results reveal that CaMKII is a Ca(2+) sensor with a key role as a feed-forward stimulator of ?-cell Ca(2+) signals that enhance GSIS under physiological and pathological conditions. PMID:24627477

Dadi, Prasanna K; Vierra, Nicholas C; Ustione, Alessandro; Piston, David W; Colbran, Roger J; Jacobson, David A

2014-05-01

413

Portal Vein Glucose Entry Triggers a Coordinated Cellular Response That Potentiates Hepatic Glucose Uptake and Storage in Normal but Not High-Fat/High-Fructose–Fed Dogs  

PubMed Central

The cellular events mediating the pleiotropic actions of portal vein glucose (PoG) delivery on hepatic glucose disposition have not been clearly defined. Likewise, the molecular defects associated with postprandial hyperglycemia and impaired hepatic glucose uptake (HGU) following consumption of a high-fat, high-fructose diet (HFFD) are unknown. Our goal was to identify hepatocellular changes elicited by hyperinsulinemia, hyperglycemia, and PoG signaling in normal chow-fed (CTR) and HFFD-fed dogs. In CTR dogs, we demonstrated that PoG infusion in the presence of hyperinsulinemia and hyperglycemia triggered an increase in the activity of hepatic glucokinase (GK) and glycogen synthase (GS), which occurred in association with further augmentation in HGU and glycogen synthesis (GSYN) in vivo. In contrast, 4 weeks of HFFD feeding markedly reduced GK protein content and impaired the activation of GS in association with diminished HGU and GSYN in vivo. Furthermore, the enzymatic changes associated with PoG sensing in chow-fed animals were abolished in HFFD-fed animals, consistent with loss of the stimulatory effects of PoG delivery. These data reveal new insight into the molecular physiology of the portal glucose signaling mechanism under normal conditions and to the pathophysiology of aberrant postprandial hepatic glucose disposition evident under a diet-induced glucose-intolerant condition. PMID:23028137

Coate, Katie C.; Kraft, Guillaume; Irimia, Jose M.; Smith, Marta S.; Farmer, Ben; Neal, Doss W.; Roach, Peter J.; Shiota, Masakazu; Cherrington, Alan D.

2013-01-01

414

Pleiotropic effects of rosuvastatin on the glucose metabolism and the subcutaneous and visceral adipose tissue behavior in C57Bl/6 mice  

PubMed Central

The aim of this study was to evaluate whether rosuvastatin (HMG-CoA reductase inhibitor) modulates the carbohydrate and lipid metabolism, the development of non-alcoholic fatty liver disease (NAFLD), and the increase in body mass in a model of diet-induced obesity. Male C57Bl/6 mice (3-months-old) were fed a high-fat diet (HF, 60% lipids) or the standard chow (SC, 10% lipids) for 15 weeks. The animals were then treated with 10 mg/kg/day (HF-R10 group), 20 mg/kg/day (HF-R20), or 40 mg/kg/day (HF-R40) of rosuvastatin for five weeks. The HF diet led to glucose intolerance, insulin resistance, weight gain, increased visceral adiposity with adipocyte hypertrophy, and hepatic steatosis (micro and macrovesicular). The rosuvastatin treatment decreased the adiposity and the adipocyte size in the HF-R10 and HF-R20 groups. In addition, rosuvastatin changed the pattern of fat distribution in the HF-R40 group because more fat was stored subcutaneously than in visceral depots. This redistribution improved the fasting glucose and the glucose intolerance. Rosuvastatin also improved the liver morphology and ultrastructure in a dose-dependent manner. In conclusion, rosuvastatin exerts pleiotropic effects through a dose-dependent improvement of glucose intolerance, insulin sensitivity and NAFLD and changes the fat distribution from visceral to subcutaneous fat depots in a mouse model of diet-induced obesity. PMID:23816341

2013-01-01

415

Contribution of clinical, metabolic, and genetic factors on hypertension in obese children and adolescents.  

PubMed

The role of ACE gene insertion (I) or deletion (D) polymorphism on blood pressure phenotype is not clear in children. The aim of this work is to examine the association between hypertension and ACE I/D polymorphism, as well as the contribution of clinical and metabolic parameters on blood pressure. The study participants were 199 obese children. Forty-four of them were hypertensive. The hypertensive subjects were older than the normotensive and most of them were pubertal. The prevalence of hypertension in obese subjects with II, ID, and DD genotype was similar. There was no difference between the hypertensive and the normotensive group according to ACE I/D genotype, BMISDS, sex, blood glucose level and total cholesterol levels. In obese children, high IR-HOMA values, puberty, presence of family history for hypertension, hypertriglyceridemia, and low HDL-cholesterol, high triglyceride/HDL-cholesterol ratio were found as increased risk factors of hypertension. In obese children and adolescents, blood pressure did not differ by ACE I/D genotype. The presence of family history, puberty, insulin resistance and hypertriglyceridemia constitute important risk factors for developing hypertension. PMID:21528810

Siklar, Zeynep; Berberoglu, Merih; Savas Erdeve, Senay; Hacihamdioglu, Bülent; Ocal, Gönül; Egin, Yonca; Akar, Nejat

2011-01-01

416

[When should secondary hypertension be suspected?].  

PubMed

Secondary hypertension is diagnosed in 5 to 10% of hypertensive patients. The probability of secondary hypertension increases, if the screening is focused on patients in which even a combination of three medicaments fails to attain the therapeutic objective, i.e. the so-called treatment-resistant hypertensives. Exclusion of secondary hypertension is part of the analysis of treatment-resistant hypertension. The most common causes of secondary hypertension are renal diseases, renal artery stenosis and primary hyperaldosteronism. PMID:19585906

Koivuviita, Niina

2009-01-01

417

Prevalence of Hypertension and Associated Risk Factors in Six Nicaraguan Communities  

PubMed Central

Objective Describe the prevalence of hypertension. Design Population based cross-sectional survey. Setting Six Nicaraguan communities with varying economies. Participants 1,355 adults aged 20–60 years who completed both self-reported and quantitative measures of health. Main Outcome Measures Prevalence of hypertension (systolic ?140 mm Hg, diastolic ?90 mm Hg, or self-reported medical history with diagnosis by a health care professional), uncontrolled hypertension (systolic ?140 mm Hg or diastolic ? 90 mm Hg), diabetes (urinary glucose excretion ?100 mg/dL or self-reported medical history diagnosed by a health care professional), and uncontrolled diabetes (urinary glucose excretion ?100 mg/dL only). Results The prevalence of hypertension was 22.0% (19.2% in men, 24.2% in women). Blood pressure was controlled in 31.0% of male hypertensives and 55.1% of female hypertensives (odds ratio [OR] 2.86; 95% confidence interval [CI] 1.74–4.69). Older age and higher body mass index were strongly associated with hypertension. Women who completed primary school had a lower risk of hypertension (OR .40; 95% CI .19–.85) compared to those with no formal education. A history of living in both urban and rural settings was associated with lower prevalence of hypertension (OR .52; 95% CI .34–.79). Diabetes mellitus was found in 1.2% of men and 4.3% of women. Male sex was independently associated with decreased risk of diabetes (OR .31; 95% CI .11–.86). Conclusions At least one cardiovascular risk factor was found in half of this Nicaraguan sample. Cardiovascular risk factors should be the target of educational efforts, screening, and treatment. PMID:22764632

Laux, Timothy S.; Bert, Philip J.; González, Marvin; Unruh, Mark; Aragon, Aurora; Lacourt, Cecilia Torres

2013-01-01

418

Human blood glucose dynamics  

E-print Network

glucose tolerance test (GTT), which has been, used heavily in the diagnosis of type II diabetes.diabetes and in the case of those with risk factors such as age and obesity, have been tested using the oral glucose tolerance test (

Rahaghi, Farbod N.

2007-01-01

419

Bilateral aplasia of the radius with abnormal hooking of the claviculae and sucrose-maltose intolerance.  

PubMed

A girl with bilateral radial aplasia, severe deformity of both hands, club foot deformity and mild anemia is described. Especially remarkable is the edging of the lateral part of the claviculae. At the same time the infant is suffering from a sucrose-maltose intolerance. PMID:7275676

Van Goethem, H; Van Goethem, C

1981-07-01

420

Computer simulation studies in fluid and calcium regulation and orthostatic intolerance  

NASA Technical Reports Server (NTRS)

The systems analysis approach to physiological research uses mathematical models and computer simulation. Major areas of concern during prolonged space flight discussed include fluid and blood volume regulation; cardiovascular response during shuttle reentry; countermeasures for orthostatic intolerance; and calcium regulation and bone atrophy. Potential contributions of physiologic math models to future flight experiments are examined.

1985-01-01