期刊论文详细信息
Nutrition & Metabolism
Mitochondriogenesis and apoptosis: possible cause of vitamin A-mediated adipose loss in WNIN/Ob-obese rats
Ayyalasomayajula Vajreswari2  Nappan V Giridharan3  Nemani Harishankar3  Lodhu Singotamu1  Shanmugam M Jeyakumar2  Anamthathmakula Prashanth2 
[1] Ultra Structure Unit, National Institute of Nutrition (ICMR), Jamai Osmania, Hyderabad -500 007, Andhra Pradesh, India;Department of Lipid Biochemistry, National Institute of Nutrition (ICMR), Jamai Osmania, Hyderabad -500 007, Andhra Pradesh, India;National Center for Laboratory Animal Sciences (ICMR), Jamai-Osmania, Hyderabad 500 007, Andhra Pradesh, India
关键词: Apoptosis;    Adipose tissue;    Nuclear receptors;    Thermogenesis;    Uncoupling protein;    Dietary supplementation;    Vitamin A;   
Others  :  1131707
DOI  :  10.1186/1743-7075-11-45
 received in 2014-06-03, accepted in 2014-09-11,  发布年份 2014
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【 摘 要 】

Background

Previously, we reported that vitamin A-enriched diet (129 mg/kg diet) intake reduces the adiposity development in obese rats of WNIN/Ob strain. Here, we hypothesize that dose lesser than 129 mg of vitamin A/kg diet would also be effective in ameliorating the development of obesity in these rats.

Methods

Five-month-old male lean and obese rats designated as A & B were divided into four subgroups (I, II, III and IV) consisting of 8 rats from each phenotype and received diets containing 2.6 mg (control group), 26 mg, 52 mg and 129 mg vitamin A/kg diet as retinyl palmitate for 20 weeks. Body composition and morphological analysis of brown adipose tissue (BAT) was analyzed. Expression of uncoupling protein 1 (UCP1), retinoic acid receptor α (RARα) and retinoid X receptor α (RXRα) in BAT and levels of Bcl2 and Bax in epididymal white adipose tissue (eWAT) were determined by immunoblotting.

Results

Vitamin A supplementation to obese rats at doses of 52 and 129 mg/kg diet showed reduced body weight gain and adiposity compared to control diet-fed obese rats receiving 2.6 mg of vitamin A/kg diet. In BAT of obese rats, vitamin A supplementation at doses of 26 and 52 mg of vitamin A/kg diet resulted in increased UCP1 expression with concomitant decrease in RARα and RXRα levels compared to control diet-fed obese rats. Further, transmission electron microscopy study revealed an increase in number of BAT mitochondria of obese rats supplemented with 26 and 52 mg of vitamin A/kg diet. Also, obese rats fed on 52 mg/kg diet resulted in increased apoptosis by altering the ratio of Bcl2 to Bax protein levels in eWAT. Notably, most of these changes were not observed in lean rats fed vitamin A-enriched diets.

Conclusion

In conclusion, chronic consumption of 52 mg of vitamin A/kg diet seems to be an effective dose in ameliorating obesity possibly through mitochondriogenesis, UCP1-mediated thermogenesis in BAT and apoptosis in eWAT of obese rats. Therefore, the role of dietary vitamin A in correcting human obesity would be of unquestionable relevance and can only be addressed by future studies.

【 授权许可】

   
2014 Prashanth et al.; licensee BioMed Central Ltd.

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