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, while showing 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 non-obese 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 (ER) transactivation activity due to elevated intra-adipose estrogens. The present study in A-AR^-/y mice suggests a differential tissue-specific role of AR in energy balance control in males.