Mo1951 Chronic Intestinal Electrical Stimulation Improves Glucose Intolerance and Insulin Resistance in Diet-Induced Obesity Rats

2016 ◽  
Vol 150 (4) ◽  
pp. S825-S826
Author(s):  
Shiying Li ◽  
Weijian Zhu ◽  
Jiande Chen
Author(s):  
Laura Gathercole ◽  
Matthew Chapman ◽  
Dean Larner ◽  
Petra Klusonova ◽  
Trevor Penning ◽  
...  

Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5826-5834 ◽  
Author(s):  
Shoshana Yakar ◽  
Nomeli P. Nunez ◽  
Patricia Pennisi ◽  
Pnina Brodt ◽  
Hui Sun ◽  
...  

Obesity increases the risk of many cancers in both males and females. This study describes a link between obesity, obesity-associated metabolic alterations, and the risk of developing cancer in male and female mice. The goal of this study was to evaluate the relationship between gender and obesity and to determine the role of estrogen status in obese females and its effect on tumor growth. We examined the susceptibility of C57BL/6 mice to diet-induced obesity, insulin resistance/glucose intolerance, and tumors. Mice were injected sc with one of two tumorigenic cell lines, Lewis lung carcinoma, or mouse colon 38-adenocarcinoma. Results show that tumor growth rate was increased in obese mice vs. control mice irrespective of the tumor cell type. To investigate the effect of estrogen status on tumor development in obese females, we compared metabolic parameters and tumor growth in ovariectomized (ovx) and intact obese female mice. Obese ovx female mice developed insulin resistance and glucose intolerance similar to that observed in obese males. Our results demonstrate that body adiposity increased in ovx females irrespective of the diet administered and that tumor growth correlated positively with body adiposity. Overall, these data point to more rapid tumor growth in obese mice and suggest that endogenous sex steroids, together with diet, affect adiposity, insulin sensitivity, and tumor growth in female mice.


2014 ◽  
Vol 289 (23) ◽  
pp. 16032-16045 ◽  
Author(s):  
Even Fjære ◽  
Ulrike L. Aune ◽  
Kristin Røen ◽  
Alison H. Keenan ◽  
Tao Ma ◽  
...  

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1785-P
Author(s):  
GUOXIAO WANG ◽  
WEIKANG CAI ◽  
THIAGO M. BATISTA ◽  
SAMIR SOFTIC ◽  
C. RONALD KAHN

2019 ◽  
Vol 317 (4) ◽  
pp. E597-E604 ◽  
Author(s):  
Martin Whitham ◽  
Martin Pal ◽  
Tim Petzold ◽  
Marit Hjorth ◽  
Casey L. Egan ◽  
...  

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.


Author(s):  
Laura Gathercole ◽  
Matthew Chapman ◽  
Dean Larner ◽  
Petra Klusonova ◽  
Trevor Penning ◽  
...  

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