FOOD SCIENCE ›› 2011, Vol. 32 ›› Issue (13): 289-292.doi: 10.7506/spkx1002-6630-201113062

• Nutrition & Hygiene • Previous Articles     Next Articles

Effects and Mechanism of Resveratrol on Body weight and Adipose Tissue Distribution of KKAy Mice

SUN Yan-shuang1, CHEN Si-fan1, ZHU Wei2, ZHENG Lin1, ZHANG Zi-li1, LING Wen-hua1,FENG Xiang1,*   

  1. (1. Guangdong Provincial Key Laboratory of Food, Nutrition and Health, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China;2. Guangzhou Center for Disease Control and Prevention, Guangzhou 510080, China)
  • Online:2011-07-15 Published:2011-07-02

Abstract: Objective: To explore the effect and mechanism of resveratrol on the body weight and adipose tissue distribution of KKAy mice. Methods: Totally 36 8-week-old KKAy mice were randomly divided into 3 groups, and fed a standard AIN93G diet or a standard AIN93G diet supplemented with resveratrol at the dose of 2 or 4 g/kg. A total of 12 C57BL/6J mice fed the standard diet were chosen as the control. The body weight, subcutaneous fat and epididymal fat of the mice were measured. The expression of silent information regulator (sirt-1), peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα) in the adipose tissue of rats were evaluated by Western blot. Results: Resveratrol could reduce the body weight of KKAy mice without dependence on food intake. Body weight and adipose tissue weight was much lower mice in the high-dose group when compared with the model group. In addition, resveratrol also enhanced the expression level of sirt-1 and inhibited the expression of PPARγ and C/EBPα in the adipose tissue of mice. Conclusion: Resveratol can ameliorate body adiposity in mice due to its promoting effect on the expression of sirt-1 in the adipose tissue and suppressive function on the expression of proteins related to lipogenesis and adipocyte differentiation.

Key words: resveratrol, adiposity, silent information regulator (sirt-1), peroxisome proliferator-activated receptor γ(PPARγ), CCAAT/enhancer-binding protein α(C/EBPα)

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