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Deletion of leptin receptors in vagal afferent neurons disrupts estrogen
signaling, body weight, food intake and hormonal controls of feeding in female
mice.

Authors	Huang KP, Ronveaux CC, de Lartigue G, Geary N, Asarian L, Raybould HE
Submitted By	Submitted Externally on 4/30/2020
Status	Published
Journal	American journal of physiology. Endocrinology and metabolism
Year	2019
Date Published	4/1/2019
Volume : Pages	316 : E568 - E577
PubMed Reference	30753113
Abstract	Deletion of the leptin receptor from vagal afferent neurons (VAN) using a conditional deletion (Nav1.8/LepRfl/fl) results in an obese phenotype with increased food intake and lack of exogenous cholecystokinin (CCK)-induced satiation in male mice. Female mice are partially protected from weight gain and increased food intake in response to ingestion of high-fat (HF) diets. However, whether the lack of leptin signaling in VAN leads to an obese phenotype or disruption of hypothalamic-pituitary-gonadal axis function in female mice is unclear. Here, we tested the hypothesis that leptin signaling in VAN is essential to maintain estrogen signaling and control of food intake, energy expenditure, and adiposity in female mice. Female Nav1.8/LepRfl/fl mice gained more weight, had increased gonadal fat mass, increased meal number in the dark phase, and increased total food intake compared with wild-type controls. Resting energy expenditure was unaffected. The decrease in food intake produced by intraperitoneal injection of CCK (3 µg/kg body wt) was attenuated in female Nav1.8/LepRfl/fl mice compared with wild-type controls. Intraperitoneal injection of ghrelin (100 µg/kg body wt) increased food intake in Nav1.8/LepRfl/fl mice but not in wild-type controls. Ovarian steroidogenesis was suppressed, resulting in decreased plasma estradiol, which was accompanied by decreased expression of estrogen receptor-1 (Esr1) in VAN but not in the hypothalamic arcuate nucleus. These data suggest that the absence of leptin signaling in VAN is accompanied by disruption of estrogen signaling in female mice, leading to an obese phenotype possibly via altered control of feeding behavior.

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