Adipose Overexpression of Desnutrin Promotes Fatty Acid Utilization and Attenuates Diet-induced Obesity
- Maryam Ahmadian, B.Sc.2,
- Robin E. Duncan, Ph.D.2,
- Krista A. Varady, Ph.D.2,
- Danubia Frasson, M.Sc.2,
- Marc K. Hellerstein, M.D., Ph.D.2,
- Andreas L. Birkenfeld, M.D.3,
- Varman T. Samuel, M.D., Ph.D.3,
- Gerald Shulman, M.D., Ph.D.3,
- Yuhui Wang, Ph.D.2,
- Chulho Kang, Ph.D.4 and
- Hei Sook Sul, Ph.D. (hsul{at}nature.berkeley.edu)2
- 2Departments of Nutritional Science and Toxicology, and
- 4Molecular and Cell Biology, University of California, Berkeley, California, 94720 USA
- 3Department of Internal Medicine, Yale University, School of Medicine, New Haven, CT, 06510 USA
Abstract
Objective: To investigate the role of desnutrin in adipose tissue triacylglycerol (TAG) and fatty acid metabolism.
Design: We generated transgenic mice overexpressing desnutrin in adipocytes (aP2-desnutrin) and also performed adenoviral-mediated overexpression of desnutrin in 3T3-L1 adipocytes.
Results: aP2-desnutrin mice were leaner with decreased adipose tissue TAG content and smaller adipocyte size. Overexpression of desnutrin increased lipolysis but did not result in increased serum fatty acid levels or ectopic TAG storage. We found increased cycling between diacylglycerol and TAG, increased fatty acid oxidation in adipocytes from these mice, as well as improved insulin sensitivity.
Conclusions: In conclusion, we show that by increasing lipolysis, desnutrin overexpression causes reduced adipocyte TAG content and attenuation of diet-induced obesity. Furthermore, desnutrin-mediated lipolysis promotes fatty acid oxidation and reesterification within adipocytes.
Footnotes
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- Received June 19, 2008.
- Accepted January 6, 2009.
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