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Science 22 November 1996:
Vol. 274. no. 5291, pp. 1377 - 1379
DOI: 10.1126/science.274.5291.1377
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Reports

Uncoupling of Obesity from Insulin Resistance Through a Targeted Mutation in aP2, the Adipocyte Fatty Acid Binding Protein

Gökhan S. Hotamisligil, * Randall S. Johnson, Robert J. Distel, Ramsey Ellis, Virginia E. Papaioannou, Bruce M. Spiegelman *

Fatty acid binding proteins (FABPs) are small cytoplasmic proteins that are expressed in a highly tissue-specific manner and bind to fatty acids such as oleic and retinoic acid. Mice with a null mutation in aP2, the gene encoding the adipocyte FABP, were developmentally and metabolically normal. The aP2-deficient mice developed dietary obesity but, unlike control mice, they did not develop insulin resistance or diabetes. Also unlike their obese wild-type counterparts, obese aP2-/- animals failed to express in adipose tissue tumor necrosis factor-alpha (TNF-alpha ), a molecule implicated in obesity-related insulin resistance. These results indicate that aP2 is central to the pathway that links obesity to insulin resistance, possibly by linking fatty acid metabolism to expression of TNF-alpha .

G. S. Hotamisligil, Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA.
R. S. Johnson, Department of Biology, University of California, San Diego, La Jolla, CA 92093, USA.
R. J. Distel, R. Ellis, B. M. Spiegelman, Dana Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
V. E. Papaioannou, Department of Genetics and Development, Columbia University, 701 West 168 Street, New York, NY 10032, USA.
*   To whom correspondence should be addressed.

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