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. 2023 Sep 15;14:20420188231199359. doi: 10.1177/20420188231199359

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© The Author(s), 2023

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 3. — Model of 17β-estradiol (E2)’s homeostatic regulation of energy balance in the brain. Brain regulation of energy homeostasis is mainly reliant on hypothalamic and brainstem-associated neuronal populations, including those in the arcuate nucleus (ARC), lateral hypothalamus (LH), ventromedial nucleus (VMN), dorsomedial nucleus, and the paraventricular nucleus, which are modulated by E2 signaling, and deliver orexigenic or anorexigenic signals to stimulate or suppress the energy intake and the energy expenditure. Proopiomelanocortin (POMC)/cocaine- and amphetamine-regulated transcript neurons and neuropeptide Y (NPY)/agouti-related peptide (AgRP) neurons in ARC may regulate the body energy status through POMC/α-melanocortin stimulating hormone signaling. POMC neurons are impinged by steroidogenic factor-1 neurons in the VMN, while NPY/AgRP neurons project to melanin-concentrating hormone neurons in LH. Nucleus tractus solitarius in the brainstem, which receives abdominal vagal afferent projections activated by the peptide cholecystokinin, may modulate the feeding inhibition effect via E2 signaling.