Document Type
Article
Publication Date
12-8-2020
Keywords
JMG
JAX Source
Elife 2020 Dec 8;9:e59616
Volume
9
ISSN
2050-084X
PMID
33289482
DOI
https://doi.org/10.7554/elife.59616
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. 17α-estradiol treatment improves metabolic parameters and slows aging in male mice. The mechanisms by which 17α-estradiol elicits these benefits remain unresolved. Herein, we show that 17α-estradiol elicits similar genomic binding and transcriptional activation through estrogen receptor α (ERα) to that of 17β-estradiol. In addition, we show that the ablation of ERα completely attenuates the beneficial metabolic effects of 17α-E2 in male mice. Our findings suggest that 17α-E2 may act through the liver and hypothalamus to improve metabolic parameters in male mice. Lastly, we also determined that 17α-E2 improves metabolic parameters in male rats, thereby proving that the beneficial effects of 17α-E2 are not limited to mice. Collectively, these studies suggest ERα may be a drug target for mitigating chronic diseases in male mammals.
Recommended Citation
Mann S,
Hadad N,
Nelson Holte M,
Rothman A,
Sathiaseelan R,
Ali Mondal S,
Agbaga M,
Unnikrishnan A,
Subramaniam M,
Hawse J,
Huffman D,
Freeman W,
Stout M.
Health benefits attributed to 17α-estradiol, a lifespan-extending compound, are mediated through estrogen receptor α. Elife 2020 Dec 8;9:e59616
Comments
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