Androgen receptor deficiency in monocytes/macrophages does not alter adiposity or glucose homeostasis in male mice
Open accessAbstract
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.
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Deletion of the AR specifically in monocytes/macrophages expressing the lysozyme 2 gene did not affect adiposity.
“Deletion of the AR specifically in monocytes/macrophages expressing the lysozyme 2 gene did not affect adiposity.”
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 [160]
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- Authors
- Rubinow, K., Houston, B., Wang, S., Goodspeed, L., Ogimoto, K., Morton, G., McCarty, C., Braun, R., & Page, S.
- Affiliations
- University of Washington (US)
- Jackson Laboratory (US)
- ORCID
- Wang, Shari
- Venue
- Asian Journal of Andrology
- Published
- 2018
- Volume
- 20
- Issue
- 3
- Pages
- 276
- ISSN
- 1008-682X (ISSN-L)
- PMC
- PMC5952483
- OpenAlex
- W2800540046
- Cited by
- 7
- References
- 48
- Citations by year
- 2024: 1 · 2022: 1 · 2021: 1 · 2020: 3 · 2019: 1
- FWCI
- 0.98
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- Asian Journal of Andrology (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Funders
- University of Washington (P30DK017047)
- Diabetes Research Center, University of Washington (P30 DK017047)
- National Heart, Lung, and Blood Institute (T32HL007028)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK017047, DK089056, P30DK035816, P30DK017047)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (U54HD042454)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- androgen receptor, monocytes/macrophages, adiposity, glucose homeostasis, insulin sensitivity, energy balance, high-fat diet, liver weight, androgen deprivation therapy, fat mass, energy expenditure
- MeSH terms
- Animals, Blood Glucose, Energy Metabolism, Glucose Tolerance Test, Homeostasis, Liver, Macrophages, Male, Monocytes, Organ Size, Receptors, Androgen, Signal Transduction, Mice, Knockout, Adiposity, Mice
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