Abstract
Metabolic dysfunction underlies several chronic diseases, many of which are exacerbated by obesity. Dietary interventions can reverse metabolic declines and slow aging, although compliance issues remain paramount. 17a-estradiol treatment improves metabolic parameters and slows aging in male mice. The mechanisms by which 17a-estradiol elicits these benefits remain unresolved. Herein, we show that 17a-estradiol elicits similar genomic binding and transcriptional activation through estrogen receptor a (ERa) to that of 17b-estradiol. In addition, we show that the ablation of ERa completely attenuates the beneficial metabolic effects of 17a-E2 in male mice. Our findings suggest that 17a-E2 may act through the liver and hypothalamus to improve metabolic parameters in male mice. Lastly, we also determined that 17a-E2 improves metabolic parameters in male rats, thereby proving that the beneficial effects of 17a-E2 are not limited to mice. Collectively, these studies suggest ERa may be a drug target for mitigating chronic diseases in male mammals.
Original language | English (US) |
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Article number | e59616 |
Pages (from-to) | 1-30 |
Number of pages | 30 |
Journal | eLife |
Volume | 9 |
DOIs | |
State | Published - Dec 2020 |
ASJC Scopus subject areas
- General Neuroscience
- General Biochemistry, Genetics and Molecular Biology
- General Immunology and Microbiology