Leptin and Corticosterone Have Opposite Effects on Food Intake and the Expression of UCP1 mRNA in Brown Adipose Tissue oflep^ob/lep^obMice

Abstract

The present study was conducted to assess the interaction effect of leptin and corticosterone on food intake and the expression of uncoupling protein 1 (UCP1) mRNA in interscapular brown adipose tissue (IBAT). To this end, a 3 x 3 factorial experiment was designed in which adrenalectomized (ADX) lep(ob)/lep(ob) mice were subjected to three doses of corticosterone and three doses of leptin. The results confirm the anorectic and orexigenic effects of leptin and corticosterone, respectively. The results also emphasize the abilities of leptin and corticosterone to respectively increase and reduce the expression of UCP1 mRNA in IBAT. The effects of leptin and corticosterone on food intake and the expression of UCP1 mRNA translated into effects on body weight and body composition; leptin reduced body weight and corticosterone increased the weight of IBAT. The present results do not provide evidence for leptin-corticosterone interactions in the control of food intake and thermogenesis. Corticosterone increased food intake and reduced the expression of IBAT UCP1 regardless of the leptin status, and leptin reduced food intake and induced the expression of IBAT UCP1 independently of the corticosterone levels.

Effects of Leptin and Corticosterone on the Expression of Corticotropin-Releasing Hormone, Agouti-Related Protein, and Proopiomelanocortin in the Brain of <i>ob/ob</i> Mouse

“…It is noteworthy that the effects of leptin and corticosterone on AGRP mRNA levels in the ARC are very consistent with the effects these hormones exert on the levels of uncoupling protein 1 in brown adipose tissue [25], which suggests that AGRP could control regulatory thermogenesis. The role of AGRP in the control of thermogenesis has not been investigated, but many reports [7, 8, 25]have emphasized the ability of glucocorticoids to reduce thermogenesis in laboratory rodents. AGRP, which is clearly overexpressed in the ob/ob mouse [18], could be a key neuropeptide in mediating the effects of glucocorticoids in the regulation of energy balance.…”

“…Obese mice were all adrenalectomized (ADX) and treated with three doses of corticosterone (provided from 100 mg cholesterol-based pellets which contained either 0, 15 or 30 mg of corticosterone) and three doses of leptin (0, 50, 100 µg/kg/day) according to a 3 × 3 factorial design [see 25]. The 9 experimental groups thus formed were labeled as follows: (1) C0-L0, (2) C0-L50, (3) C0-L100, (4) C15-L0, (5) C15-L50, (6) C15-L100, (7) C30-L0, (8) C30-L50 and (9) C30-L100.…”

“…It has recently been demonstrated that glucocorticoids could acutely prevent the anorectic action of leptin [22]and chronically impair the effect of the latter on energy balance [23]. In contrast, it has also been reported that leptin could lead to the expression of uncoupling protein 1 and prevent fat deposition, even in presence of moderate levels of corticosterone [23, 24, 25]. The present study was designed to assess the respective and interactive effects of leptin and corticosterone on the expression of CRH, POMC and AGRP mRNA in adrenalectomized ob/ob mice treated with various doses of leptin and corticosterone.…”

Sexual Dimorphism in Adipose-Hypothalamic Crosstalk and the Contribution of Aryl Hydrocarbon Receptor to Regulate Energy Homeostasis

“…Moreover, males also have increased sympathetic neuronal projections and postsynaptic adrenergic receptors in VAT [ 165 , 166 ]. Glucocorticoids can also suppress BAT activity, by downregulating thermogenic gene expression [ 167 ]. Corticosterone treatment not only increases lipid accumulation, but also decreases catecholamine-induced UCP1 expression in BAT in both male and female mice [ 168 , 169 , 170 , 171 ].…”

The role of 5‐HT2c receptor on corticosterone‐mediated food intake

“…Corticosterone, the main adrenal hormone secreted in response to hypothalamic–pituitary–adrenal (HPA) axis activity, exerts feedback effects in the hypothalamus in rodents . Corticosterone increased food consumption, which has the opposite effects on food intake as that produced by leptin . However, acute stress has been reported to reduce cumulative food intake, while increasing corticosterone in rodents .…”