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Endocrinology, doi:10.1210/en.2007-0516
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Endocrinology Vol. 149, No. 5 2361-2368
Copyright © 2008 by The Endocrine Society

Hyperleptinemia without Obesity in Male Mice Lacking Androgen Receptor in Adipose Tissue

I-Chen Yu1, Hung-Yun Lin1, Ning-Chun Liu, Ruey-Shen Wang, Janet D. Sparks, Shuyuan Yeh and Chawnshang Chang

Departments of Pathology, Urology, and Neuroscience, George Whipple Laboratory for Cancer Research, and the Cancer Center, University of Rochester Medical Center, Rochester, New York 14642

Address all correspondence and requests for reprints to: Chawnshang Chang, Ph.D., 601 Elmwood Avenue, Box 626, Rochester, New York 14642. E-mail: chang{at}urmc.rochester.edu.

Insulin resistance occurs through an inadequate response to insulin by insulin target organs such as liver, muscle, and adipose tissue with consequent insufficient glucose uptake. In previous studies we demonstrated that whole body androgen receptor (AR) knockout (AR–/y) mice develop obesity and exhibit insulin and leptin resistance at advanced age. By examining adipose tissue-specific AR knockout (A-AR–/y) mice, we found A-AR–/y mice were hyperleptinemic but showed no leptin resistance, although body weight and adiposity index of A-AR–/y mice were identical with those of male wild-type control mice. Hypotriglyceridemia and hypocholesterolemia found in nonobese A-AR–/y mice suggested a beneficial effect of high leptin levels independent of fat deposition. Further examination showed that androgen-AR signaling in adipose tissue plays a direct regulatory role in leptin expression via enhanced estrogen receptor transactivation activity due to elevated intraadipose estrogens. The present study in A-AR–/y mice suggests a differential tissue-specific role of AR in energy balance control in males.






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Copyright © 2008 by The Endocrine Society