Sustained activation of PPARα by endogenous ligands increases hepatic fatty acid oxidation and prevents obesity in ob/ob mice
Sustained activation of PPARα by endogenous ligands increases hepatic fatty acid oxidation and prevents obesity in ob/ob mice
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DOI：
10.1096/fj.11-194019
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发表时间：
2012-02-01
期刊：
影响因子：
4.8
通讯作者：
Reddy, Janardan K.
中科院分区：
文献类型：
--
作者：
Huang, Jiansheng;Jia, Yuzhi;Reddy, Janardan K.
Obesity, a major health concern, results from an imbalance between energy intake and expenditure. Leptin-deficient ob/ob mice are paradigmatic of obesity, resulting from excess energy intake and storage. Mice lacking acyl-CoA oxidase 1 (Acox1), the first enzyme of the peroxisomal fatty acid beta-oxidation system, are characterized by increased energy expenditure and a lean body phenotype caused by sustained activation of peroxisome proliferator-activated receptor alpha (PPAR alpha) by endogenous ligands in liver that remain unmetabolized in the absence of Acox1. We generated ob/ob mice deficient in Acox1 (Acox1(-/-)) to determine how the activation of PPAR alpha by endogenous ligands might affect the obesity of ob/ob mice. In contrast to Acox1(-/-) (14.3 +/- 1.2 g at 6 mo) and the Acox1-deficient (ob/ob) double-mutant mice (23.8 +/- 4.6 g at 6 mo), the ob/ob mice are severely obese (54.3 +/- 3.2 g at 6 mo) and had significantly more (P
