Selective estrogen signaling key to postmenopausal risk of obesity
- Date:
- January 18, 2011
- Source:
- Journal of Clinical Investigation
- Summary:
- Although the hormone estradiol-17-beta is a key reproductive hormone, it also contributes to the regulation of energy balance and body weight. As a result, estrogen deficiency following menopause is associated with an increased probability of obesity. New research has generated data that suggest it might be possible to develop drugs that selectively reduce the risks of obesity and metabolic disturbances in postmenopausal women.
- Share:
The hormone estradiol-17-beta is a key reproductive hormone. However, it also contributes to the regulation of energy balance and body weight. As a result, estrogen deficiency following menopause is associated with an increased probability of obesity and increased risk for developing type 2 diabetes.
A team of researchers, led by Jon Levine, at Northwestern University, Evanston, has now generated new insight into the mechanisms by which ER-alpha signaling maintains normal energy balance. Specifically, the team found that nonclassical ER-alpha signaling is key to the effects of estradiol-17-beta on energy balance.
These data lead them to suggest that it might be possible to develop drugs that selectively activate nonclassical ER-alpha signaling to reduce the risks of obesity and metabolic disturbances in postmenopausal women.
The research appears in the Journal of Clinical Investigation.
Story Source:
Materials provided by Journal of Clinical Investigation. Note: Content may be edited for style and length.
Journal Reference:
- Cheryl J. Park, Zhen Zhao, Christine Glidewell-Kenney, Milos Lazic, Pierre Chambon, Andrée Krust, Jeffrey Weiss, Deborah J. Clegg, Andrea Dunaif, J. Larry Jameson, Jon E. Levine. Genetic rescue of nonclassical ER-alpha signaling normalizes energy balance in obese Er-alpha-null mutant mice. Journal of Clinical Investigation, 2011; DOI: 10.1172/JCI41702
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