Ghrelin receptor signaling is not required for glucocorticoid-induced obesity in female mice

Chronic exposure to high circulating glucocorticoid or ghrelin concentrations increases food intake, weight gain and adiposity, suggesting that could contribute the metabolic effects of chronic glucocorticoids. In male mice, however, blocking receptor (GHSR) signaling increased adiposity induced by corticosterone (CORT), rather than attenuating them. current study, we investigated role GHSR in CORT female mice. To do this, WT KO mice were treated with either a 1% ethanol (EtOH) solution EtOH alone their drinking water for 32 days ( n = 5–8/group). Body weight, food, intake as well vaginal cyclicity assessed daily. As expected, treatment-induced significant body also impaired glucose tolerance. contrast results observed did not differ on any these parameters. Neither plasma levels ghrelin, LEAP-2, endogenous antagonist produced liver, nor ratio altered exposure. addition, treatment disrupted cyclicity, reduction sucrose consumption locomotor activity regardless genotype. decreased exploration but Collectively, data suggest most metabolic, endocrine, reproductive behavioral are independent