Distinct role of adiposity and insulin resistance in glucose intolerance: Studies in ventromedial hypothalamic-lesioned obese rats

Metabolism ◽  
2002 ◽  
Vol 51 (6) ◽  
pp. 716-723 ◽  
Author(s):  
Asako Kageyama ◽  
Tsutomu Hirano ◽  
Haruaki Kageyama ◽  
Toshimasa Osaka ◽  
Yoshio Namba ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Intolerance ◽  
Obese Rats ◽  
Distinct Role

Botryosphaeran reduces obesity, hepatic steatosis, dyslipidaemia, insulin resistance and glucose intolerance in diet-induced obese rats

Life Sciences ◽  
2018 ◽  
Vol 211 ◽  
pp. 147-156 ◽  
Author(s):  
Amadeu Z. Silva ◽  
Felipe P.L. Costa ◽  
Ingrid L. Souza ◽  
Mariana C. Ribeiro ◽  
Morenna Alana Giordani ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Glucose Intolerance ◽  
Obese Rats

scholarly journals The Essential Role of PRAK in Preserving Cardiac Function and Insulin Resistance in High-Fat Diet-Induced Diabetes

2021 ◽  
Vol 22 (15) ◽  
pp. 7995
Author(s):  
Jianfeng Du ◽  
Yu Tina Zhao ◽  
Hao Wang ◽  
Ling X. Zhang ◽  
Gangjian Qin ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Cardiac Function ◽  
Western Blot ◽  
Glucose Intolerance ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
Wild Type ◽  
High Fat

Regulated/activated protein kinase (PRAK) plays a crucial role in modulating biological function. However, the role of PRAK in mediating cardiac dysfunction and metabolic disorders remains unclear. We examined the effects of deletion of PRAK on modulating cardiac function and insulin resistance in mice exposed to a high-fat diet (HFD). Wild-type and PRAK−/− mice at 8 weeks old were exposed to either chow food or HFD for a consecutive 16 weeks. Glucose tolerance tests and insulin tolerance tests were employed to assess insulin resistance. Echocardiography was employed to assess myocardial function. Western blot was used to determine the molecular signaling involved in phosphorylation of IRS-1, AMPKα, ERK-44/42, and irisin. Real time-PCR was used to assess the hypertrophic genes of the myocardium. Histological analysis was employed to assess the hypertrophic response, interstitial myocardial fibrosis, and apoptosis in the heart. Western blot was employed to determine cellular signaling pathway. HFD-induced metabolic stress is indicated by glucose intolerance and insulin intolerance. PRAK knockout aggravated insulin resistance, as indicated by glucose intolerance and insulin intolerance testing as compared with wild-type littermates. As compared with wild-type mice, hyperglycemia and hypercholesterolemia were manifested in PRAK-knockout mice following high-fat diet intervention. High-fat diet intervention displayed a decline in fractional shortening and ejection fraction. However, deletion of PRAK exacerbated the decline in cardiac function as compared with wild-type mice following HFD treatment. In addition, PRAK knockout mice enhanced the expression of myocardial hypertrophic genes including ANP, BNP, and βMHC in HFD treatment, which was also associated with an increase in cardiomyocyte size and interstitial fibrosis. Western blot indicated that deletion of PRAK induces decreases in phosphorylation of IRS-1, AMPKα, and ERK44/42 as compared with wild-type controls. Our finding indicates that deletion of PRAK promoted myocardial dysfunction, cardiac remodeling, and metabolic disorders in response to HFD.

The Infant Born to a Woman with Gestational Diabetes

2017 ◽  
Vol 36 (4) ◽  
pp. 239-244 ◽  
Author(s):  
Theresa Povinelli ◽  
Caitlin Lim ◽  
Deborah A. Raines
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Amino Acids ◽  
Gestational Diabetes ◽  
Glucose Tolerance ◽  
Gestational Diabetes Mellitus ◽  
Glucose Intolerance ◽  
Frequent Episodes ◽  
Altered Glucose

AbstractGestational diabetes mellitus (GDM) is defined as glucose intolerance with onset during pregnancy. During pregnancy, women with GDM develop insulin resistance, which results in altered glucose tolerance. As a result, there are frequent episodes of hyperglycemia and high levels of circulating amino acids, increasing the transfer of nutrients to the fetus. This article discusses the role of the mother–baby nursing in the care of neonates born to women with gestational diabetes.

scholarly journals Adipocyte-specific deletion of IL-6 does not attenuate obesity-induced weight gain or glucose intolerance in mice

2019 ◽  
Vol 317 (4) ◽  
pp. E597-E604 ◽  
Author(s):  
Martin Whitham ◽  
Martin Pal ◽  
Tim Petzold ◽  
Marit Hjorth ◽  
Casey L. Egan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Glucose Intolerance ◽  
Genetic Model ◽  
Whole Body ◽  
Littermate Control ◽  
Diet Induced Obesity ◽  
Marked Weight ◽  
Liver Insulin Resistance

It has been suggested that interleukin-6 (IL-6) produced by adipocytes in obesity leads to liver insulin resistance, although this hypothesis has never been definitively tested. Accordingly, we did so by generating adipocyte-specific IL-6-deficient (AdipoIL-6−/−) mice and studying them in the context of diet-induced and genetic obesity. Mice carrying two floxed alleles of IL-6 (C57Bl/6J) were crossed with Cre recombinase-overexpressing mice driven by the adiponectin promoter to generate AdipoIL-6−/− mice. AdipoIL-6−/− and floxed littermate controls were fed a standard chow or high-fat diet (HFD) for 16 wk and comprehensively metabolically phenotyped. In addition to a diet-induced obesity model, we also examined the role of adipocyte-derived IL-6 in a genetic model of obesity and insulin resistance by crossing the AdipoIL-6−/− mice with leptin-deficient ( ob/ob) mice. As expected, mice on HFD and ob/ob mice displayed marked weight gain and increased fat mass compared with chow-fed and ob/+ (littermate control) animals, respectively. However, deletion of IL-6 from adipocytes in either model had no effect on glucose tolerance or fasting hyperinsulinemia. We concluded that adipocyte-specific IL-6 does not contribute to whole body glucose intolerance in obese mice.

scholarly journals Insulin Resistance in Chronic Kidney Disease: Is There a Distinct Role of Vitamin D?

2021 ◽  
Vol 24 (2) ◽  
pp. 128-134
Author(s):  
Heba Attea ◽  
Alaa El Din Abd El Hamid ◽  
Mohammed Keshawy ◽  
Mohamed Khedr
Keyword(s):  
Insulin Resistance ◽  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Distinct Role
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