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

CORNEJO MP; VALDIVIA S; GARCÍA ROMERO G; DE FRANCESCO PN; ANDREOLI MF; LAZZARINO G; REYNALDO M; RAMOS G; PERELLÓ M

Buenos Aires

Congreso; 2nd Congress of the Federation of Latin-American and Caribbean Societies for Neuroscience (FALAN); 2016

Federation of Latin-American and Caribbean Societies for Neuroscience

A variety of human eating disordersdisplay binge eating events, which involve the consumption of large amounts offood in a discrete period of time. Ghrelin is the only peptide hormone known toincrease food intake, and its receptor (GHSR) is a G-protein coupled receptorcapable of signal in a ghrelin-independent manner. The central distribution ofGHSR indicates that ghrelin system regulates both homeostatic and hedonicaspects of feeding. Using a simple model of binge eating, in which ad libitumfed mice are exposed to high fat diet (HFD) 4 consecutive days for 2 h/day, wehave shown that mice develop a HFD intake escalation over the successive eventsthat involve the activation of the mesolimbic system and ghrelin signaling.Here, we tested if ghrelin-evoked GHSR signaling is required for the HFD intakeescalation and we found that the pharmacologic blockage of ghrelin signalingfailed to affect HFD intake escalation. Interestingly, mice eating HFD 2 h/dayfor 4 successive days display an increase in GHSR levels in the ventraltegmental area (VTA), as well as an increase in c-Fos levels in thedopaminergic neurons of the VTA and in the nucleus accumbens. Unexpectedly, wefound that mice with GHSR expression limited to the dopaminergic neurons failedto show HFD intake escalation. Thus, we conclude that food intake escalation inmice daily exposed to HFD involves ghrelin-independent GHSR signaling in asubset of neurons different from the dopaminergic neurons of the VTA.