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Abstract

Volume 20, Issue 3 (May 2018) 20, 276–283; 10.4103/aja.aja_54_17

Androgen receptor deficiency in monocytes/macrophages does not alter adiposity or glucose homeostasis in male mice

Katya B Rubinow1, Barbara Houston1, Shari Wang1, Leela Goodspeed1, Kayoko Ogimoto1, Gregory J Morton1, Christopher McCarty2, Robert E Braun2, Stephanie T Page1

1 Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA 98195, USA
2 Jackson Laboratory, Bar Harbor, ME 04609, USA

Correspondence: Dr. KB Rubinow (rubinow@uw.edu)

05-Dec-2017

Abstract

Androgen deprivation in men leads to increased adiposity, but the mechanisms underlying androgen regulation of fat mass have not been fully defined. Androgen receptor (AR) is expressed in monocytes/macrophages, which are resident in key metabolic tissues and influence energy metabolism in surrounding cells. Male mice bearing a cell-specific knockout of the AR in monocytes/macrophages (M-ARKO) were generated to determine whether selective loss of androgen signaling in these cells would lead to altered body composition. Wild-type (WT) and M-ARKO mice (12–22 weeks of age, n = 12 per group) were maintained on a regular chow diet for 8 weeks and then switched to a high-fat diet for 8 additional weeks. At baseline and on both the regular chow and high-fat diets, no differences in lean mass or fat mass were observed between groups. Consistent with the absence of differential body weight or adiposity, no differences in food intake (3.0 ± 0.5 g per day for WT mice vs 2.8 ± 0.4 g per day for M-ARKO mice) or total energy expenditure (0.6 ± 0.1 Kcal h−1 for WT mice vs 0.5 ± 0.1 Kcal h−1 for M-ARKO mice) were evident between groups during high-fat feeding. Liver weight was greater in M-ARKO than that in WT mice (1.5 ± 0.1 g vs 1.3 ± 0.0 g, respectively, P = 0.02). Finally, M-ARKO mice did not exhibit impairments in glucose tolerance or insulin sensitivity relative to WT mice at any study time point. In aggregate, these findings suggest that AR signaling specifically in monocytes/macrophages does not contribute to the regulation of systemic energy balance, adiposity, or insulin sensitivity in male mice.

Keywords: androgen receptor; knockout mice; macrophages; male hypogonadism; metabolic syndrome

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