Developmental changes in hypothalamic SF-1, POMC, and ERα mRNA expression and their sensitivity to fasting in male and female rats

Iwasa, Takeshi; Matsuzaki, Takashi; Mayila, Yiliyasi; Yano, Kiyohito; Irahara, Minoru

doi:10.1507/endocrj.ej17-0140

Cited by 7 publications

(1 citation statement)

References 13 publications

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“…These results extend the understanding about estrogenic actions on feeding regulations, which could be bidirectional depending on the internal energy state and contribute to the maintenance of energy homeostasis in face of various environmental challenges. Although E2 levels and the expression of ERα in the hypothalamus may not undergo dynamic changes during the fasting–feeding transition in normal females [ 71 ], our finding that E2 and ERα signals are required for female animals to properly respond to hunger provided new mechanistic insights on the association of abnormal feeding behavior with irregular estrogen levels in certain medical conditions that disproportionally affect women, such as anorexia nervosa [ [72] , [73] , [74] ], and therefore may facilitate the development of suitable therapeutic strategies for these conditions.…”

Section: Discussionmentioning

confidence: 99%

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

Hyseni

et al. 2020

Molecular Metabolism

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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-AF2 0 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-AF2 0 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.

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Section: Discussionmentioning

confidence: 99%