期刊
ELIFE
卷 9, 期 -, 页码 -出版社
eLIFE SCIENCES PUBL LTD
DOI: 10.7554/eLife.59616
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资金
- National Institutes of Health [R00 AG51661, R01 AG059430, R01 EY030513, T32 AG052363, R01 AG069742]
- Harold Hamm Diabetes Center
- Veterans Affairs Oklahoma City [I01BX003906]
- University of Oklahoma Health Sciences Center [P30 EY012190]
- Einstein Nathan Shock Center [P30 AG038072]
- NATIONAL INSTITUTE ON AGING [R01AG069742] Funding Source: NIH RePORTER
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. 17 alpha-estradiol treatment improves metabolic parameters and slows aging in male mice. The mechanisms by which 17 alpha-estradiol elicits these benefits remain unresolved. Herein, we show that 17 alpha-estradiol elicits similar genomic binding and transcriptional activation through estrogen receptor alpha (ER alpha) to that of 17 beta-estradiol. In addition, we show that the ablation of ER alpha completely attenuates the beneficial metabolic effects of 17 alpha-E2 in male mice. Our findings suggest that 17 alpha-E2 may act through the liver and hypothalamus to improve metabolic parameters in male mice. Lastly, we also determined that 17 alpha-E2 improves metabolic parameters in male rats, thereby proving that the beneficial effects of 17 alpha-E2 are not limited to mice. Collectively, these studies suggest ER alpha may be a drug target for mitigating chronic diseases in male mammals.
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