期刊
SCIENTIFIC REPORTS
卷 6, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep23459
关键词
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资金
- NIH [Baylor College of Medicine] [R01DK093587, R01DK101379, R00DK085330]
- USDA ARS/CRIS Award [6250-51000- 055]
- American Diabetes Association
- American Heart Association postdoctoral fellowship
- American Heart Association National Scientist Development Grant
- National Natural Science Foundation of China Award (Baylor College of Medicine) [81200623]
- USDA ARS
- NIH [Cedars-Sinai Medical Center] [F31 HL128054, P01 DK088761]
- NIH [University of Texas Health Science Center at Houston] [R01DK092605]
Estrogens act in the ventromedial hypothalamic nucleus (VMH) to regulate body weight homeostasis. However, the molecular mechanisms underlying these estrogenic effects are unknown. We show that activation of estrogen receptor-alpha (ER alpha) stimulates neural firing of VMH neurons expressing ERa, and these effects are blocked with intracellular application of a pharmacological inhibitor of the phosphatidyl inositol 3-kinase (PI3K). Further, we demonstrated that mice with genetic inhibition of PI3K activity in VMH neurons showed a sexual dimorphic obese phenotype, with only female mutants being affected. In addition, inhibition of VMH PI3K activity blocked effects of 17 beta-estradiol to stimulate energy expenditure, but did not affect estrogen-induced anorexia. Collectively, our results indicate that PI3K activity in VMH neurons plays a physiologically relevant role in mediating estrogenic actions on energy expenditure in females.
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