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Diabetes 54:1000-1008, 2005
© 2005 by the American Diabetes Association, Inc.

Androgen Receptor Null Male Mice Develop Late-Onset Obesity Caused by Decreased Energy Expenditure and Lipolytic Activity but Show Normal Insulin Sensitivity With High Adiponectin Secretion

WuQiang Fan1, Toshihiko Yanase1, Masatoshi Nomura1, Taijiro Okabe1, Kiminobu Goto1, Takashi Sato2, Hirotaka Kawano2, Shigeaki Kato2, and Hajime Nawata1

1 Department of Medicine and Bioregulatory Science, Graduate School of Medical Science, Kyushu University, Fukuoka, Japan
2 Institute of Molecular and Cellular Biosciences, Graduate School of Agricultural and Life Sciences, University of Tokyo, Tokyo, Japan

Androgen receptor (AR) null male mice (ARL–/Y) revealed late-onset obesity, which was confirmed by computed tomography–based body composition analysis. ARL–/Y mice were euphagic compared with the wild-type male (ARX/Y) controls, but they were also less dynamic and consumed less oxygen. Transcript profiling indicated that ARL–/Y mice had lower transcripts for the thermogenetic uncoupling protein 1, which was subsequently found to be ligand-dependently activated by AR. We also found enhanced secretion of adiponectin, which is insulin sensitizing, from adipose tissue and a relatively lower expression of peroxisome proliferator–activated receptor-{gamma} in white adipose tissue in comparison to ARX/Y mice. Both factors might explain why the overall insulin sensitivity of ARL–/Y mice remained intact, despite their apparent obesity. The results revealed that AR plays important roles in male metabolism by affecting the energy balance, and it is negative to both adiposity and insulin sensitivity.

Address correspondence and reprint requests to Toshihiko Yanase, MD, PhD, Department of Medicine and Bioregulatory Science, Graduate School of Medical Science, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582 Japan. E-mail: yanase{at}intmed3.med.kyushu-u.ac.jp


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