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Androgen Receptor Null Male Mice Develop Late-Onset Obesity Caused by Decreased Energy Expenditure and Lipolytic Activity but Show Normal Insulin Sensitivity With High Adiponectin Secretion
Open accessAbstract
Androgen receptor (AR) null male mice (ARL−/Y) revealed late-onset obesity, which was confirmed by computed tomography–based body composition analysis. ARL−/Y mice were euphagic compared with the wild-type male (ARX/Y) controls, but they were also less dynamic and consumed less oxygen. Transcript profiling indicated that ARL−/Y mice had lower transcripts for the thermogenetic uncoupling protein 1, which was subsequently found to be ligand-dependently activated by AR. We also found enhanced secretion of adiponectin, which is insulin sensitizing, from adipose tissue and a relatively lower expression of peroxisome proliferator–activated receptor-γ in white adipose tissue in comparison to ARX/Y mice. Both factors might explain why the overall insulin sensitivity of ARL−/Y mice remained intact, despite their apparent obesity. The results revealed that AR plays important roles in male metabolism by affecting the energy balance, and it is negative to both adiposity and insulin sensitivity.
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Metadata
- Authors
- Fan, W., Yanase, T., Nomura, M., Okabe, T., Goto, K., Sato, T., Kawano, H., Kato, S., & Nawata, H.
- Affiliations
- Kyushu University (JP)
- The University of Tokyo (JP)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-04-01
- Volume
- 54
- Issue
- 4
- Pages
- 1000-1008
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2027264386
- Cited by
- 269
- References
- 45
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 15 · 2023: 8 · 2022: 18 · 2021: 13 · 2020: 11 · 2019: 6 · 2018: 18 · 2017: 21 · 2016: 17 · 2015: 18 · 2014: 16 · 2013: 15 · 2012: 11
- FWCI
- 5.99
- Type
- journal article
- Language
- en
- Open access
- green
- pure.teikyo.jp
- Licence
- cc-by-nc-nd
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- androgen receptor, late-onset obesity, energy expenditure, lipolysis, insulin sensitivity, adiponectin secretion, UCP1, thermogenesis, PPARγ, white adipose tissue, energy balance, euphoria
- MeSH terms
- Uncoupling Protein 1, Adipose Tissue, Aging, Animals, Body Weight, Carrier Proteins, Energy Metabolism, Insulin, Insulin Resistance, Ion Channels, Lipolysis, Male, Membrane Proteins, Obesity, Oxygen Consumption, Receptors, Androgen, Gene Expression, Mice, Knockout, Mitochondrial Proteins, Intercellular Signaling Peptides and Proteins, Mice, Adiponectin
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