scholarly journals Methodological considerations when studying the skeletal response to glucose intolerance using the diet-induced obesity model

2016 ◽  
Vol 5 ◽  
Author(s):  
Elizabeth Rendina-Ruedy ◽  
Brenda J Smith
Keyword(s):  
Glucose Intolerance ◽  
Diet Induced Obesity ◽  
Methodological Considerations

Female 5[beta]-reductase knockout mice are protected from diet induced obesity, insulin resistance and glucose intolerance

2016 ◽  
Author(s):  
Laura Gathercole ◽  
Matthew Chapman ◽  
Dean Larner ◽  
Petra Klusonova ◽  
Trevor Penning ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Intolerance ◽  
Knockout Mice ◽  
Diet Induced Obesity

scholarly journals Increased Tumor Growth in Mice with Diet-Induced Obesity: Impact of Ovarian Hormones

Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5826-5834 ◽  
Author(s):  
Shoshana Yakar ◽  
Nomeli P. Nunez ◽  
Patricia Pennisi ◽  
Pnina Brodt ◽  
Hui Sun ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Tumor Growth ◽  
Glucose Intolerance ◽  
Tumor Development ◽  
Tumor Growth Rate ◽  
Obese Mice ◽  
Female Mice ◽  
Diet Induced Obesity ◽  
Body Adiposity ◽  
Obese Female

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.

Broccoli extract improves high fat diet-induced obesity, hepatic steatosis and glucose intolerance in Wistar rats

2019 ◽  
Vol 59 ◽  
pp. 319-328 ◽  
Author(s):  
Paula Aranaz ◽  
David Navarro-Herrera ◽  
Ana Romo-Hualde ◽  
María Zabala ◽  
Miguel López-Yoldi ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Wistar Rats ◽  
High Fat ◽  
Diet Induced Obesity

scholarly journals Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance

2014 ◽  
Vol 56 (2) ◽  
pp. 379-389 ◽  
Author(s):  
Taylor Banh ◽  
David W. Nelson ◽  
Yu Gao ◽  
Ting-Ni Huang ◽  
Mei-I Yen ◽  
...  
Keyword(s):  
Glucose Intolerance ◽  
Adult Onset ◽  
Diet Induced Obesity

scholarly journals The host response to poly(lactide-co-glycolide) scaffolds protects mice from diet induced obesity and glucose intolerance

Biomaterials ◽  
2019 ◽  
Vol 217 ◽  
pp. 119281 ◽  
Author(s):  
Michael A. Hendley ◽  
Kendall P. Murphy ◽  
Christopher Isely ◽  
Heather L. Struckman ◽  
Prakasam Annamalai ◽  
...  
Keyword(s):  
Glucose Intolerance ◽  
Host Response ◽  
Diet Induced Obesity

scholarly journals The Development of Diet-Induced Obesity and Glucose Intolerance in C57Bl/6 Mice on a High-Fat Diet Consists of Distinct Phases

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e106159 ◽  
Author(s):  
Lynda M. Williams ◽  
Fiona M. Campbell ◽  
Janice E. Drew ◽  
Christiane Koch ◽  
Nigel Hoggard ◽  
...  
Keyword(s):  
Glucose Intolerance ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity

scholarly journals Postnatal treatment with metyrapone attenuates the effects of diet-induced obesity in female rats exposed to early-life stress

2017 ◽  
Vol 312 (2) ◽  
pp. E98-E108 ◽  
Author(s):  
Margaret O. Murphy ◽  
Joseph B. Herald ◽  
Caleb T. Wills ◽  
Stanley G. Unfried ◽  
Dianne M. Cohn ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Glucose Intolerance ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Female Rats ◽  
Male Rats ◽  
Female Rat ◽  
Diet Induced Obesity ◽  
Postnatal Treatment

Experimental studies in rodents have shown that females are more susceptible to exhibiting fat expansion and metabolic disease compared with males in several models of fetal programming. This study tested the hypothesis that female rat pups exposed to maternal separation (MatSep), a model of early-life stress, display an exacerbated response to diet-induced obesity compared with male rats. Also, we tested whether the postnatal treatment with metyrapone (MTP), a corticosterone synthase inhibitor, would attenuate this phenotype. MatSep was performed in WKY offspring by separation from the dam (3 h/day, postnatal days 2–14). Upon weaning, male and female rats were placed on a normal (ND; 18% kcal fat) or high-fat diet (HFD; 60% kcal fat). Nondisturbed littermates served as controls. In male rats, no diet-induced differences in body weight (BW), glucose tolerance, and fat tissue weight and morphology were found between MatSep and control male rats. However, female MatSep rats displayed increased BW gain, fat pad weights, and glucose intolerance compared with control rats ( P < 0.05). Also, HFD increased plasma corticosterone (196 ± 51 vs. 79 ± 18 pg/ml, P < 0.05) and leptin levels (1.8 ± 0.4 vs. 1.3 ± 0.1 ng/ml, P < 0.05) in female MatSep compared with control rats, whereas insulin and adiponectin levels were similar between groups. Female control and MatSep offspring were treated with MTP (50 µg/g ip) 30 min before the daily separation. MTP treatment significantly attenuated diet-induced obesity risk factors, including elevated adiposity, hyperleptinemia, and glucose intolerance. These findings show that exposure to stress hormones during early life could be a key event to enhance diet-induced obesity and metabolic disease in female rats. Thus, pharmacological and/or behavioral inflection of the stress levels is a potential therapeutic approach for prevention of early life stress-enhanced obesity and metabolic disease.

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