High fat intake in a mouse binge eating model may involve constitutive ghrelin receptor signaling

CORNEJO PAULA; VALDIVIA SPRING; GARCÍA ROMERO GUADALUPE; DE FRANCESCO NICOLÁS; ANDREOLI M. F.; LAZZARINO, GISELA; REYNALDO MIRTA; RAMOS, J. GUILLERMO; PERELLO MARIO

Buenos Aires

Congreso; 2nd FALAN congress; 2016

Sociedad Argentina de Neurociencias-Federation of Latin American and Caribbean Neuroscience

A variety of human eating disorders display binge eating events, which involve the consumption of large amounts of food in a discrete period of time. Ghrelin is the only peptide hormone known to increase food intake, and its receptor (GHSR) is a Gprotein coupled receptor capable of signal in a ghrelinindependent manner. The central distribution of GHSR indicates that ghrelin system regulates both homeostatic and hedonic aspects of feeding. Using a simple model of binge eating, in which ad libitum fed mice are exposed to high fat diet (HFD) 4 consecutive days for 2 h/day, we have shown that mice develop a HFD intake escalation over the successive events that involve the activation of the mesolimbic system and ghrelin signaling. Here, we tested if ghrelinevoked GHSR signaling is required for the HFD intake escalation and we found that the pharmacologic blockage of ghrelin signaling failed to affect HFD intake escalation. Interestingly, mice eating HFD 2 h/day for 4 successive days display an increase in GHSR levels in the ventral tegmental area (VTA), as well as an increase in cFos levels in the dopaminergic neurons of the VTA and in the nucleus accumbens. Unexpectedly, we found that mice with GHSR expression limited to the dopaminergic neurons failed to show HFD intake escalation. Thus, we conclude that food intake escalation in mice daily exposed to HFD involves ghrelinindependent GHSR signaling in a subset of neurons different from the dopaminergic neurons of the VTA.