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Am J Physiol Endocrinol Metab 295: E331-E338, 2008. First published May 27, 2008; doi:10.1152/ajpendo.00577.2007
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Loss of resistin ameliorates hyperlipidemia and hepatic steatosis in leptin-deficient mice

Neel S. Singhal,1,3 Rajesh T. Patel,1,2 Yong Qi,1,2 Yun-Sik Lee,1,2 and Rexford S. Ahima1,2,3

1Division of Endocrinology, Diabetes and Metabolism; 2Institute for Diabetes, Obesity and Metabolism; and 3Neuroscience Graduate Group, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Submitted 6 September 2007 ; accepted in final form 26 May 2008

Resistin has been linked to components of the metabolic syndrome, including obesity, insulin resistance, and hyperlipidemia. We hypothesized that resistin deficiency would reverse hyperlipidemia in genetic obesity. C57Bl/6J mice lacking resistin [resistin knockout (RKO)] had similar body weight and fat as wild-type mice when fed standard rodent chow or a high-fat diet. Nonetheless, hepatic steatosis, serum cholesterol, and very low-density lipoprotein (VLDL) secretion were decreased in diet-induced obese RKO mice. Resistin deficiency exacerbated obesity in ob/ob mice, but hepatic steatosis was drastically attenuated. Moreover, the levels of triglycerides, cholesterol, insulin, and glucose were reduced in ob/ob-RKO mice. The antisteatotic effect of resistin deficiency was related to reductions in the expression of genes involved in hepatic lipogenesis and VLDL export. Together, these results demonstrate a crucial role of resistin in promoting hepatic steatosis and hyperlipidemia in obese mice.

adipocytokine; lipoprotein; triglyceride; cholesterol


Address for reprint requests and other correspondence: R. Ahima, Univ. of Pennsylvania School of Medicine, Div. of Endocrinology, Diabetes and Metabolism, 415 Curie Blvd., 712A Clinical Research Bldg., Philadelphia, PA 19104 (email: ahima{at}mail.med.upenn.edu)






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