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Deletion of PPARγ in Adipose Tissues of Mice Protects against High Fat Diet-Induced Obesity and Insulin Resistance
Julie R. Jones, Cordelia Barrick, Kyoung-Ah Kim, Jill Lindner, Bertrand Blondeau, Yuka Fujimoto, Masakazu Shiota, Robert A. Kesterson, Barbara B. Kahn, Mark A. Magnuson and Jeffrey M. Friedman
Proceedings of the National Academy of Sciences of the United States of America
Vol. 102, No. 17 (Apr. 26, 2005), pp. 6207-6212
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/3375278
Page Count: 6
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Peroxisome proliferator-activated receptor γ (PPARγ) plays a crucial role in adipocyte differentiation, glucose metabolism, and other physiological processes. To further explore the role of PPARγ in adipose tissues, we used a Cre/loxP strategy to generate adipose-specific PPARγ knockout mice. These animals exhibited marked abnormalities in the formation and function of both brown and white adipose tissues. When fed a high-fat diet, adipose-specific PPARγ knockout mice displayed diminished weight gain despite hyperphagia, had diminished serum concentrations of both leptin and adiponectin, and did not develop glucose intolerance or insulin resistance. Characterization of in vivo glucose dynamics pointed to improved hepatic glucose metabolism as the basis for preventing high-fat diet-induced insulin resistance. Our findings further illustrate the essential role for PPARγ in the development of adipose tissues and suggest that a compensatory induction of hepatic PPARγ may stimulate an increase in glucose disposal by the liver.
Proceedings of the National Academy of Sciences of the United States of America © 2005 National Academy of Sciences