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17?-estradiol promotes acute refeeding in hungry mice via membrane-initiated ER? signaling.

ABSTRACT: OBJECTIVE:Estrogen protects animals from obesity through estrogen receptor ? (ER?), 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 17?-estradiol (E2) and ER? 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. ER?-C451A mutant mice deficient in membrane-bound ER? activity and ER?-AF20 mutant mice lacking ER? 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 ER? mutations on the neural activities of ER? neurons in the hypothalamus. RESULTS:In the wild-type female mice, ovariectomy reduced fasting-induced refeeding, which was restored by E2 supplementation. The ER?-C451A mutation, but not the ER?-AF20 mutation, attenuated acute feeding induced by either fasting or central glucopenia. The ER?-C451A mutation consistently impaired the neural responses of hypothalamic ER? 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 ER? activity.

SUBMITTER: Yu K

PROVIDER: S-EPMC7484552 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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17β-estradiol promotes acute refeeding in hungry mice via membrane-initiated ERα signaling.

Yu Kaifan K He Yanlin Y Hyseni Ilirjana I Pei Zhou Z Yang Yongjie Y Xu Pingwen P Cai Xing X Liu Hesong H Qu Na N Liu Hailan H He Yang Y Yu Meng M Liang Chen C Yang Tingting T Wang Julia J Gourdy Pierre P Arnal Jean-Francois JF Lenfant Francoise F Xu Yong Y Wang Chunmei C

Molecular metabolism 20200723

<h4>Objective</h4>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.<h4>Methods</h4>Wild-type female mice with surgical depletion of endogenous estrogens were used to ...[more]

PMID: 32712433

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Project description:Graphical abstract Highlights • The role and mechanism of 17β -estradiol in the regulation of BMSC promoting angiogenesis were analyzed by bioinformatics techniques for the first time.• Combined with FN1, MCM2, XPO1, NTRK1 and other proteins, 17β-estradiol is able to activate PI3K-Akt, MAPK and other signaling pathways to regulate BMSCs to promote or remodel angiogenesis.• 17β-estradiol upregulates the PI3K-Akt signaling pathway to promote the BMSC angiogenesis process of differentiation. Objective Estrogen is an important hormone affecting angiogenesis in women and is important for female physical development. Menopausal women are prone to serious cardiovascular and cerebrovascular diseases when estrogen is significantly reduced. Bone marrow mesenchymal stem cells (BMSC) have potential roles in processes such as angiogenesis and remodeling. This study is to investigate the effect of 17β-estradiol on BMSC angiogenic differentiation and its underlying molecular mechanism, and to provide a basis for the treatment of microvascular diseases. Methods Enrichment analysis of apoptosis, migration or angiogenesis processes and molecular mechanisms of BMSC treated with 17β-estradiol was performed to screen core proteins and perform molecular docking validation. Human MSCs were cultured in vitro to examine the effect of 17β-estradiol on BMSC migration or angiogenic differentiation. Results 17β-estradiol acted on 48 targets of BMSC and was involved in regulating 52 cell migration processes or 17 angiogenesis processes through 66 KEGG pathways such as PI3K-Akt, MAPK, etc. 17β-estradiol bound tightly to 10 core proteins including APP, NTRK1, EGFR, and HSP90AA1. 17β-estradiol promoted cell scratch area closure rate and CD31 expression in BMSCs, downregulated BMSC apoptosis rate, and promoted Akt and p-Akt protein expression in BMSC. Conclusion 17β-estradiol binds to FN1, MCM2, XPO1, NTRK1 and other proteins to initiate PI3K-Akt, MAPK and other signaling pathways, so as to regulate BMSC to promote or remodel angiogenesis, verifying that 17β-estradiol up-regulates PI3K-Akt signaling pathway to promote BMSC angiogenic differentiation.

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17?-estradiol promotes acute refeeding in hungry mice via membrane-initiated ER? signaling.

Publications

17β-estradiol promotes acute refeeding in hungry mice via membrane-initiated ERα signaling.

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