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Article
Nature Medicine  7, 941 - 946 (2001)
doi:10.1038/90984

The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity

T. Yamauchi1, J. Kamon1, H. Waki1, Y. Terauchi1, N. Kubota1, K. Hara1, Y. Mori2, T. Ide3, K. Murakami3, N. Tsuboyama-Kasaoka4, O. Ezaki4, Y. Akanuma5, O. Gavrilova6, C. Vinson7, M.L. Reitman6, H. Kagechika8, K. Shudo8, M. Yoda9, Y. Nakano9, K. Tobe1, R. Nagai1, S. Kimura1, M. Tomita9, P. Froguel2 & T. Kadowaki1

1  Department of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan

2  Institute of Biology-CNRS, Pasteur Institute of Lille, Lille, France

3  Central Research Laboratories, Kyorin Pharmaceutical, Tochigi, Japan

4  Division of Clinical Nutrition, National Institute of Health and Nutrition, Tokyo, Japan

5  Institute for Diabetes Care and Research, Asahi Life Foundation, Tokyo, Japan

6  Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, Bethesda, Maryland, USA

7  Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

8  Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan

9  Department of Physiological Chemistry, School of Pharmaceutical Sciences, Showa University, Tokyo, Japan

Correspondence should be addressed to T. Kadowaki kadowaki-3im@h.u-tokyo.ac.jp
Adiponectin is an adipocyte-derived hormone. Recent genome-wide scans have mapped a susceptibility locus for type 2 diabetes and metabolic syndrome to chromosome 3q27, where the gene encoding adiponectin is located. Here we show that decreased expression of adiponectin correlates with insulin resistance in mouse models of altered insulin sensitivity. Adiponectin decreases insulin resistance by decreasing triglyceride content in muscle and liver in obese mice. This effect results from increased expression of molecules involved in both fatty-acid combustion and energy dissipation in muscle. Moreover, insulin resistance in lipoatrophic mice was completely reversed by the combination of physiological doses of adiponectin and leptin, but only partially by either adiponectin or leptin alone. We conclude that decreased adiponectin is implicated in the development of insulin resistance in mouse models of both obesity and lipoatrophy. These data also indicate that the replenishment of adiponectin might provide a novel treatment modality for insulin resistance and type 2 diabetes.

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Nature Medicine
ISSN: 1078-8956
EISSN: 1546-170X
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