17β-estradiol promotes acute refeeding in hungry mice via membrane-initiated ERα signaling
| Autor: | Chunmei Wang, Pingwen Xu, Françoise Lenfant, Zhou Pei, Tingting Yang, Ilirjana Hyseni, Hesong Liu, Chen Liang, Xing Cai, Yanlin He, Pierre Gourdy, Yong Xu, Meng Yu, Julia Wang, Yang He, Jean-François Arnal, Kaifan Yu, Hailan Liu, Yongjie Yang, Na Qu |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty lcsh:Internal medicine medicine.drug_class Hunger Ovariectomy Mutant Hypothalamus Estrogen receptor 030209 endocrinology & metabolism Endogeny Hypoglycemia Biology medicine.disease_cause Energy homeostasis 03 medical and health sciences Mice 0302 clinical medicine E2 Internal medicine medicine Animals Homeostasis Obesity lcsh:RC31-1245 Molecular Biology ERα Mutation Estradiol Feeding Estrogen Receptor alpha Cell Biology Feeding Behavior medicine.disease Mice Inbred C57BL 030104 developmental biology Endocrinology Estrogen Glucose-sensing Female Original Article Signal Transduction |
| Zdroj: | Molecular Metabolism, Vol 42, Iss, Pp 101053-(2020) Molecular Metabolism |
| ISSN: | 2212-8778 |
| Popis: | Objective Estrogen protects animals from obesity through estrogen receptor α (ERα), partially by inhibiting overeating in animals fed ad libitum. However, the effects of estrogen on feeding behavior in hungry animals remain unclear. In this study, we examined the roles of 17β-estradiol (E2) and ERα in the regulation of feeding in hungry female animals and explored the underlying mechanisms. Methods Wild-type female mice with surgical depletion of endogenous estrogens were used to examine the effects of E2 supplementation on acute refeeding behavior after starvation. ERα-C451A mutant mice deficient in membrane-bound ERα activity and ERα-AF20 mutant mice lacking ERα transcriptional activity were used to further examine mechanisms underlying acute feeding triggered by either fasting or central glucopenia (induced by intracerebroventricular injections of 2-deoxy-D-glucose). We also used electrophysiology to explore the impact of these ERα mutations on the neural activities of ERα neurons in the hypothalamus. Results In the wild-type female mice, ovariectomy reduced fasting-induced refeeding, which was restored by E2 supplementation. The ERα-C451A mutation, but not the ERα-AF20 mutation, attenuated acute feeding induced by either fasting or central glucopenia. The ERα-C451A mutation consistently impaired the neural responses of hypothalamic ERα neurons to hypoglycemia. Conclusion In addition to previous evidence that estrogen reduces deviations in energy balance by inhibiting eating at a satiated state, our findings demonstrate the unexpected role of E2 that promotes eating in hungry mice, also contributing to the stability of energy homeostasis. This latter effect specifically requires membrane-bound ERα activity. Highlights • Endogenous E2 is required to maintain acute refeeding in hungry female mice after starvation. • Membrane-bound ERα activity in female mice is required for efficient refeeding after starvation. • Membrane-bound ERα activity is required for hypothalamic ERα neurons to respond to hypoglycemia. |
| Databáze: | OpenAIRE |
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