Involvement of Sex, Strain and Age Factors in High Fat Diet-Induced Obesity in C57BL/6J and BALB/cA Mice

Nishikawa, Satomi; Yasoshima, Akira; Doi, Kunio; Nakayama, Hiroyuki; Uetsuka, Koji

doi:10.1538/expanim.56.263

Cited by 171 publications

(167 citation statements)

References 20 publications

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“…[12][13][14][15] High-fat diets and excessive food consumption increase the amount of body fat and promote insulin resistance in humans and mice. 18,19 Our studies show findings similar to other published results: obese mice consuming a HF diet gained high levels of body fat and became insulin resistant when compared with mice consuming a LF diet or a CR regimen. Results also show that alcohol-consuming mice had lower fasting blood glucose levels compared with water-consuming mice.…”

Section: Discussionsupporting

confidence: 90%

“…31,34 In their studies, however, rats consumed an ethanol-containing liquid diet, which contained high levels of fat. 32,34 Our results (Figure 3a) and those of others 19,35 show that a HFdiet can induce insulin resistance. Therefore, it is possible that the combination of alcohol and high lipid content in the liquid diet can lead to insulin resistance.…”

Section: Discussionsupporting

confidence: 77%

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Alcohol consumption promotes insulin sensitivity without affecting body fat levels

et al. 2009

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Objective: Alcohol consumption promotes insulin sensitivity. In obesity, a decrease in body fat levels decreases the risk of developing insulin resistance; therefore, it is possible that alcohol improves insulin sensitivity by negatively affecting body fat. The aim of this study was to determine whether alcohol consumption promotes insulin sensitivity by reducing body fat levels in C57BL/6 male mice. Methods: We examined the effects of alcohol consumption on insulin sensitivity in male mice with three different body weight (BW) phenotypes. The BWs were induced by feeding the mice a 30% calorie-restricted (CR) regimen, a low-fat (LF) diet and a high-fat (HF) diet. The mice had free access to water or 20% ethanol in the drinking water. To determine the effects of the three different BW phenotypes and of alcohol on glucose regulation and insulin sensitivity, we performed the insulin tolerance test (ITT) and glucose tolerance test (GTT) on the mice. The effects of the diets and alcohol on body composition, percent body fat (% BF), percent lean mass and bone mineral density (BMD) were determined by dual-energy X-ray absorptiometry (DEXA). Results: Data show that mice with the highest body fat levels (HF) were insulin resistant and glucose intolerant. In contrast, mice with the lowest body fat levels (CR) were the most insulin sensitive and cleared the injected endogenous glucose the fastest. Results show that alcohol did not affect GTT in any of the BW phenotypes. However, alcohol consumption promoted insulin sensitivity in mice consuming both the LF and HF diets. Alcohol consumption increased insulin sensitivity without affecting body fat levels, as body fat levels were similar in mice consuming the LF or HF diets and drinking either water or alcohol. Conclusions: Alcohol consumption promotes insulin sensitivity without affecting body fat levels in mice consuming LF and HF diets.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 77%

Alcohol consumption promotes insulin sensitivity without affecting body fat levels

et al. 2009

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“…5-fold changes between KO and WT control mice (Supplementary Figures 1B, C and 2). Sexual dimorphism in HFD-induced obesity and metabolic alterations, and hepatic transport of taurocholate have been reported in mice and rats (Simon et al 1999, Nishikawa et al 2007, Hwang et al 2010, Grove et al 2010. In humans, key characteristics of obesity such as pattern of fat accumulation, energy homeostasis, and sensitivity of the brain to adiposity hormones, insulin and leptin, have been shown to be influenced by gender (Woods et al 2003, Regitz-Zagrosek et al 2007.…”

Section: Discussionmentioning

confidence: 99%

Gender-dependent effect of Gpbar1 genetic deletion on the metabolic profiles of diet-induced obese mice

Vassileva

Hu²,

Hoos³

et al. 2010

Journal of Endocrinology

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G-protein-coupled bile acid receptor 1 (GPBAR1/TGR5/ M-Bar/GPR131) is a cell surface receptor involved in the regulation of bile acid metabolism. We have previously shown that Gpbar1-null mice are resistant to cholesterol gallstone disease when fed a lithogenic diet. Other published studies have suggested that Gpbar1 is involved in both energy homeostasis and glucose homeostasis. Here, we examine the functional role of Gpbar1 in diet-induced obese mice. We found that body weight, food intake, and fasted blood glucose levels were similar between Gpbar1-null mice and their wild-type (WT) littermates when fed a chow or high-fat diet (HFD) for 2 months. However, insulin tolerance tests revealed improved insulin sensitivity in male Gpbar1 K/K mice fed chow, but impaired insulin sensitivity when fed a HFD. In contrast, female Gpbar1 K/K mice exhibited improved insulin sensitivity when fed a HFD compared with their WT littermates. Female Gpbar1 K/K mice had significantly lower plasma cholesterol and triglyceride levels than their WT littermates on both diets. Male Gpbar1 K/K mice on HFD displayed increased hepatic steatosis when compared with Gpbar1 C/C males and Gpbar1 K/K females on HFD. These results suggest a gender-dependent regulation of Gpbar1 function in metabolic disease.

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“…We previously observed that HFD-induced hepatic lipid accumulation is more severe in BALB/c mice than in B6 mice Toxicologic Pathology, 40: 71-82, 2012 Copyright # 2012 by The Author(s) ISSN: 0192-6233 print / 1533-1601 online DOI: 10.1177/0192623311422078 (Nishikawa et al 2007;Nishikawa et al 2008). In this study we analyzed changes in gene expression and histopathological patterns as well as important metabolic changes underlying the development of hepatic steatosis.…”

Section: Introductionmentioning

confidence: 99%

Gene Expression in Livers of BALB/C and C57BL/6J Mice Fed a High-Fat Diet

Nishikawa¹,

Sugimoto²,

Okada³

et al. 2011

Toxicol Pathol

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We previously demonstrated that high-fat diet (HFD)-induced hepatic lipid accumulation is more severe in BALB/c mice than in C57BL/ 6J (B6) mice. To understand the changes in liver metabolism, we studied blood chemistry, gene expression, and histopathological changes of the liver in nine-week HFD-fed BALB/c and B6 mice and one-or four-week HFD-fed BALB/c mice. Serum total cholesterol and triglyceride levels were significantly increased in all HFD-fed groups, and one-and four-week HFD-fed BALB/c groups, respectively. Histopathology revealed that vacuolation of hepatocytes was severe in nine-week HFD-fed BALB/c mice, although it was less severe in the other groups. Microarray analysis of mRNA expression of nine-week HFD-fed BALB/c mice showed up-regulation of genes involved in fatty acid uptake and biosynthesis, such as Cd36, Acaca, Acly, and Fasn. Some changes were observed in the one-and four-week HFD-fed BALB/c groups and the nine-week HFD-fed B6 group, however these changes in mRNA expression were not so marked. In conclusion, the fatty accumulation observed in BALB/c mice may be caused, at least in part, by up-regulation of fatty acid uptake and biosynthesis. Cd36, Acaca, Acly and Fasn may be involved in these metabolic processes.

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Involvement of Sex, Strain and Age Factors in High Fat Diet-Induced Obesity in C57BL/6J and BALB/cA Mice

Cited by 171 publications

References 20 publications

Alcohol consumption promotes insulin sensitivity without affecting body fat levels

Alcohol consumption promotes insulin sensitivity without affecting body fat levels

Gender-dependent effect of Gpbar1 genetic deletion on the metabolic profiles of diet-induced obese mice

Gene Expression in Livers of BALB/C and C57BL/6J Mice Fed a High-Fat Diet

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