Impact of the ghrelin signaling on food intake after a fasting event

ALEXANDRA LABARTHE; FLORENCIA ACUTAIN; VIRGINIE TOLLE; FERNANDEZ, GIMENA; GUADALUPE GARCIA ROMERO; AGUSTINA CABRAL; MIRTA REYNALDO; FLORENCIA ANDREOLI; JACQUES EPELBAUM; GUILLERMO RAMOS; MARIO PERELLO

Buenos Aires

Congreso; 2nd Congreso de la Federación de Asociaciones Latinoamericanas y del Caribe de Neurociencias (FALAN); 2016

Refeeding after a period of severe fasting triggers a robust hyperphagia, which persists even after animals have reached their energy needs. Plasma ghrelin levels and the hypothalamic gene expression of the ghrelin receptor (or growth hormone secretagogue receptor, GHSR) increase during fasting in order to cope with the negative energy balance condition. Here, we investigated the potential modulatory role of the ghrelin system on the compensatory hyperphagia that display mice that have been exposed to a 48h fasting period. Using automated feeding/activity stations in mice exposed to a fast-refeeding paradigm, we found that refed wild-type mice display a significant increase of the total food intake that continues for 6 days after refeeding. GHSR-deficient mice also show a compensatory hyperphagia, which was significantly smaller than observed in wild-type mice. Fasted wild-type mice show an increase of plasma ghrelin levels as well as an increase of the GHSR levels in the hypothalamic arcuate nucleus, as indicated by both a ghrelin binding assay and gene expression analysis. Notably, plasma ghrelin levels return to basal levels 1 day after refeeding while hypothalamic GHSR levels seems to remain increased even after 4 days of refeeding. Thus, we conclude that the ghrelin system plays a modulatory role on the magnitude of the hyperphagia observed after a severe fasting period. Supported by PICTO 2013-0065.