Estrogen and androgen receptors: regulators of fuel homeostasis and emerging targets for diabetes and obesity
Open accessAbstract
Because of increasing life expectancy, the contribution of age-related estrogen or androgen deficiency to obesity and type 2 diabetes will become a new therapeutic challenge. This review integrates current concepts on the mechanisms through which estrogen receptors (ERs) and androgen receptor (AR) regulate energy homeostasis in rodents and humans. In females, estrogen maintains energy homeostasis via ERα and ERβ, by suppressing energy intake and lipogenesis, enhancing energy expenditure, and ameliorating insulin secretion and sensitivity. In males, testosterone is converted to estrogen and maintains fuel homeostasis via ERs and AR, which share related functions to suppress adipose tissue accumulation and improve insulin sensitivity. We suggest that ERs and AR could be potential targets in the prevention of age-related metabolic disorders.
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Estrogen deficiency enhances metabolic dysfunction predisposing to type 2 diabetes, metabolic syndrome, and cardiovascular diseases.
“Disturbances of this metabolic signal lead to the development of metabolic syndrome and a higher cardiovascular risk in women.”
From Estrogen deficiency and the origin of obesity during menopause (2014) · cites this paper as [32]
Several physiological systems exhibit ultradian rhythms in the 1-3 h range, including the HPG axis, HPA axis, and suprachiasmatic nucleus.
“Several physiological systems exhibit ultradian rhythms (URs) in the 1–3 h range, including the HPG axis60–65, the HPA axis66–72, and the suprachiasmatic nucleus73, 74 – the principal orchestrating brain area for circadian rhythms.”
From Maternal and Early-Life Circadian Disruption Have Long-Lasting Negative Consequences on Offspring Development and Adult Behavior in Mice (2017) · cites this paper as [61]
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Lundholm, L., Bryzgalova, G., Gao, H., Portwood, N., Fält, S., Berndt, K. D., Dicker, A., Galuska, D., Zierath, J. R., Gustafsson, J., et al. (2008) · Journal of Endocrinology · doi:10.1677/joe-08-0192 · Cited by 71 · see citing works
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Fan, W., Yanase, T., Nishi, Y., Chiba, S., Okabe, T., Nomura, M., Yoshimatsu, H., Kato, S., Takayanagi, R., & Nawata, H. (2008) · Endocrinology · doi:10.1210/en.2008-0431 · Cited by 32 · see citing works
Paik, S. G., Michelis, M. A., Kim, Y. T., et al. (1982) · Diabetes · doi:10.2337/diabetes.31.8.724 · Cited by 26 · see citing works
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Sex and gender: modifiers of health, disease, and medicine
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GLP-1/glucagon receptor co-agonism for treatment of obesity
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Lassance, L., Haghiac, M., Minium, J., Catalano, P., & Hauguel-de Mouzon, S. (2015) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2014-2792 · Cited by 73 · see citing works
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Smarr, B. L., Zucker, I., & Kriegsfeld, L. J. (2016) · PLOS ONE · doi:10.1371/journal.pone.0160127 · Cited by 54 · see citing works
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Chen, K. L. A., Zhao, Y. C., Hieronymi, K., Smith, B. P., & Madak-Erdogan, Z. (2017) · PLOS ONE · doi:10.1371/journal.pone.0189911 · Cited by 19 · see citing works
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20-Hydroxyecdysone activates the protective arm of the renin angiotensin system via Mas receptor
Lafont, R., Raynal, S., Serova, M., Didry-Barca, B., Guibout, L., Latil, M., Dilda, P. J., Dioh, W., & Veillet, S. (2020) · doi:10.1101/2020.04.08.032607 · Cited by 11 · see citing works
Black, M. N., Wilkinson, J. A., Webb, E. K., Kamal, M., Bahniwal, R., McGlory, C., Phillips, S. M., & Devries, M. C. (2021) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00878.2019 · Cited by 6 · see citing works
- Authors
- Mauvais-Jarvis, F.
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2011-01
- Volume
- 22
- Issue
- 1
- Pages
- 24-33
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC3011051
- OpenAlex
- W2021664357
- Cited by
- 335
- References
- 100
- Citations by year
- 2026: 20 · 2025: 23 · 2024: 16 · 2023: 20 · 2022: 28 · 2021: 28 · 2020: 19 · 2019: 23 · 2018: 22 · 2017: 30 · 2016: 19 · 2015: 14 · 2014: 23 · 2013: 18 · 2012: 19
- FWCI
- 1.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK074970)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P50HD044405)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- estrogen receptor alpha, estrogen receptor beta, androgen receptor, energy homeostasis, type 2 diabetes, obesity, insulin sensitivity, insulin secretion, lipogenesis, energy expenditure, testosterone, adipose tissue accumulation, metabolic disorders
- MeSH terms
- Animals, Diabetes Mellitus, Female, Homeostasis, Humans, Male, Obesity, Receptors, Androgen, Receptors, Estrogen
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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