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Cited by 180Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismLipid metabolism and biosynthesis

Understanding androgen action in adipose tissue

O’Reilly, Michael W., House, Philip J., Tomlinson., Jeremy W.·2014·The Journal of Steroid Biochemistry and Molecular Biology
DOI 10.1016/j.jsbmb.2014.04.008
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Abstract

Androgens play an important role in regulation of body fat distribution in humans. They exert direct effects on adipocyte differentiation in a depot-specific manner, via the androgen receptor (AR), leading to modulation of adipocyte size and fat compartment expansion. Androgens also impact directly on key adipocyte functions including insulin signalling, lipid metabolism, fatty acid uptake and adipokine production. Androgen excess and deficiency have implications for metabolic health in both males and females, and these metabolic effects may be mediated through adipose tissue via effects on fat distribution, adipocyte function and lipolysis. Research into the field of androgen metabolism in human and animal adipose tissue has produced inconsistent results; it is important to take into account the sex-, depot- and organism-specific effects of androgens in fat. In general, studies point towards a stimulatory effect on lipolysis, with impairment of adipocyte differentiation, insulin signalling and adipokine generation. Observed effects are frequently gender-specific. Adipose tissue is an important organ of pre-receptor androgen metabolism, through which local androgen availability is rigorously controlled. Adipose androgen exposure is tightly controlled by isoenzymes of AKR1C, 5α-reductase and others, but regulation of the balance between generation and irreversible inactivation remains poorly understood. In particular, AKR1C2 and AKR1C3 are crucial in the regulation of local androgen bioavailability within adipose tissue. These isoforms control the balance between activation of androstenedione (A) to testosterone (T) by the 17β-hydroxysteroid dehydrogenase activity (17β-HSD) of AKR1C3, or inactivation of 5α-dihydrotestosterone (DHT) to 5α-androstane-3α,17β-diol by the 3α-hydroxysteroid dehydrogenase (3α-HSD) activity of AKR1C2. Most studies suggest that androgen inactivation is the predominant reaction in fat, particularly in the abdominal subcutaneous (SC) depot. Modulation of local adipose androgen availability may afford future therapeutic options to improve metabolic phenotype in disorders of androgen excess and deficiency.

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Authors
O’Reilly, M. W., House, P. J., & Tomlinson., J. W.
Affiliations
University of Birmingham (GB)
Corresponding author
O’Reilly, Michael W.
ORCID
Venue
The Journal of Steroid Biochemistry and Molecular Biology
Publisher
Elsevier BV
Published
2014-09
Volume
143
Pages
277-284
ISSN
0960-0760 (ISSN-L)
DOI
10.1016/j.jsbmb.2014.04.008
OpenAlex
W2000467286
Cited by
180
References
115
Citations by year
2026: 14 · 2025: 20 · 2024: 17 · 2023: 11 · 2022: 20 · 2021: 10 · 2020: 21 · 2019: 14 · 2018: 20 · 2017: 10 · 2016: 7 · 2015: 10 · 2014: 6
FWCI
1.47
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • The Journal of Steroid Biochemistry and Molecular Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Wellcome Trust (099909)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords
androgens, adipose tissue, androgen receptor, adipogenesis, body fat distribution, insulin signaling, lipid metabolism, adipokines, lipolysis, androgen metabolism, AKR1C2, AKR1C3, 17β-hydroxysteroid dehydrogenase, 3α-hydroxysteroid dehydrogenase, 5α-reductase, hyperandrogenism, androgen deficiency, sex differences, subcutaneous abdominal fat
MeSH terms
Adipose Tissue, Androgens, Animals, Female, Humans, Male

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