Article abstract
Nature Medicine 15, 159 - 168 (2009)
Published online: 11 January 2009 | doi:10.1038/nm.1904
AdPLA ablation increases lipolysis and prevents obesity induced by high-fat feeding or leptin deficiency
Kathy Jaworski1,4, Maryam Ahmadian1,4, Robin E Duncan1,4, Eszter Sarkadi-Nagy1, Krista A Varady1, Marc K Hellerstein1, Hui-Young Lee2, Varman T Samuel2, Gerald I Shulman2, Kee-Hong Kim3, Sarah de Val1, Chulho Kang3 & Hei Sook Sul1
Abstract
A main function of white adipose tissue is to release fatty acids from stored triacylglycerol for other tissues to use as an energy source. Whereas endocrine regulation of lipolysis has been extensively studied, autocrine and paracrine regulation is not well understood. Here we describe the role of the newly identified major adipocyte phospholipase A2, AdPLA (encoded by Pla2g16, also called HREV107), in the regulation of lipolysis and adiposity. AdPLA-null mice have a markedly higher rate of lipolysis owing to increased cyclic AMP levels arising from the marked reduction in the amount of adipose prostaglandin E2 that binds the G
i-coupled receptor, EP3. AdPLA-null mice have markedly reduced adipose tissue mass and triglyceride content but normal adipogenesis. They also have higher energy expenditure with increased fatty acid oxidation within adipocytes. AdPLA-deficient ob/ob mice remain hyperphagic but lean, with increased energy expenditure, yet have ectopic triglyceride storage and insulin resistance. AdPLA is a major regulator of adipocyte lipolysis and is crucial for the development of obesity.
- Department of Nutritional Science and Toxicology, 220 Morgan Hall, University of California, Berkeley, California 94720, USA.
- Department of Internal Medicine, 333 Cedar Street, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
- Department of Molecular and Cell Biology, 447 Life Sciences Addition #2751, University of California, Berkeley, California 94720, USA.
- These authors contributed equally to this work.
Correspondence to: Hei Sook Sul1 e-mail: hsul@nature.berkeley.edu
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