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Cited by 78Hormonal and reproductive studiesRegulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic Diseases

Increased adiposity in DNA binding-dependent androgen receptor knockout male mice associated with decreased voluntary activity and not insulin resistance

Rana, Kesha, Fam, Barbara C., Clarke, Michele V., Pang, Tammy P. S., Zajac, Jeffrey D., MacLean, Helen E.·2011·American Journal of Physiology-Endocrinology and Metabolism
DOI 10.1152/ajpendo.00584.2010
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Abstract

In men, as testosterone levels decrease, fat mass increases and muscle mass decreases. Increased fat mass in men, in particular central obesity, is a major risk factor for type 2 diabetes, cardiovascular disease, and all-cause mortality. Testosterone treatment has been shown to decrease fat mass and increase fat-free mass. We hypothesize that androgens act directly via the DNA binding-dependent actions of the androgen receptor (AR) to regulate genes controlling fat mass and metabolism. The aim of this study was to determine the effect of a global DNA binding-dependent (DBD) AR knockout (DBD-ARKO) on the metabolic phenotype in male mice by measuring body mass, fat mass, food intake, voluntary physical activity, resting energy expenditure, substrate oxidation rates, serum glucose, insulin, lipid, and hormone levels, and metabolic gene expression levels and second messenger protein levels. DBD-ARKO males have increased adiposity despite a decreased total body mass compared with wild-type (WT) males. DBD-ARKO males showed reduced voluntary activity, decreased food intake, increased serum leptin and adiponectin levels, an altered lipid metabolism gene profile, and increased phosphorylated CREB levels compared with WT males. This study demonstrates that androgens acting via the DNA binding-dependent actions of the AR regulate fat mass and metabolism in males and that the increased adiposity in DBD-ARKO male mice is associated with decreased voluntary activity, hyperleptinemia and hyperadiponectinemia and not with insulin resistance, increased food intake, or decreased resting energy expenditure.

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  • ARKO mice develop obesity with increased adipocyte numbers and visceral fat mass suggesting that fat is androgen-responsive.

    “Briefly, ARKO mice develop obesity with increased adipocyte numbers and visceral fat mass suggesting that fat is androgen-responsive.35”

    From Lowered testosterone in male obesity: Mechanisms, morbidity and management (2014) · cites this paper as [35]

  • An obese phenotype of increased subcutaneous and visceral fat mass as well as increased numbers of larger adipocytes have been reported in ARKOs fed a regular chow diet from 9-12 weeks of age.

    “An obese phenotype of increased subcutaneous and visceral fat mass as well as increased numbers of larger adipocytes have been reported in ARKOs fed a regular chow diet from 9–12 weeks of age.”

    From The role of the androgen receptor in the pathogenesis of obesity and its utility as a target for obesity treatments (2022) · cites this paper as [144]

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Authors
Rana, K., Fam, B. C., Clarke, M. V., Pang, T. P. S., Zajac, J. D., & MacLean, H. E.
Affiliations
The University of Melbourne (AU)
Corresponding author
MacLean, Helen E.
ORCID
Zajac, Jeffrey D.
Venue
American Journal of Physiology-Endocrinology and Metabolism
Publisher
American Physiological Society
Published
2011-11
Volume
301
Issue
5
Pages
E767-E778
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
DOI
10.1152/ajpendo.00584.2010
OpenAlex
W2153799853
Cited by
78
References
62
Citations by year
2026: 4 · 2025: 3 · 2024: 3 · 2023: 1 · 2022: 3 · 2021: 6 · 2020: 4 · 2019: 5 · 2018: 6 · 2017: 4 · 2016: 10 · 2015: 8 · 2014: 11 · 2013: 4 · 2012: 6
FWCI
5.51
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
androgen receptor, adiposity, fat mass, voluntary physical activity, dietary intake, leptin, adiponectin, CREB phosphorylation, lipid metabolism, resting energy expenditure, substrate oxidation, insulin resistance, testosterone, male mice, metabolic gene expression
MeSH terms
Animals, DNA, DNA-Binding Proteins, Eating, Insulin Resistance, Male, Mice, Inbred C57BL, Motivation, Motor Activity, Receptors, Androgen, Down-Regulation, Up-Regulation, Mice, Knockout, Leptin, Adiposity, Mice, Adiponectin, Protein Interaction Domains and Motifs

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