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

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 exh...

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Bibliographic Details
Published in:Endocrinology (Philadelphia) 2008-05, Vol.149 (5), p.2361-2368
Main Authors: Yu, I-Chen, Lin, Hung-Yun, Liu, Ning-Chun, Wang, Ruey-Shen, Sparks, Janet D, Yeh, Shuyuan, Chang, Chawnshang
Format: Article
Language:English
Subjects:
3T3-L1 Cells
Adipose Tissue - metabolism
Animals
Biological and medical sciences
Body Fat Distribution
Cells, Cultured
Embryo, Mammalian
Energy Metabolism - genetics
Fibroblasts - metabolism
Fundamental and applied biological sciences. Psychology
Integrases - genetics
Leptin - blood
Leptin - secretion
Lipid Metabolism - genetics
Lipids - blood
Male
Medical sciences
Metabolic diseases
Metabolic Diseases - genetics
Metabolic Diseases - metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Obesity
Obesity - blood
Obesity - genetics
Organ Specificity - genetics
Oxidation-Reduction
Receptors, Androgen - genetics
Receptors, Androgen - metabolism
Vertebrates: endocrinology
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Summary: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.
ISSN:0013-7227
1945-7170
DOI:10.1210/en.2007-0516