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

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

Buenos Aires

Congreso; 2nd FALAN congress; 2016

A variety of human eating disordersdisplay binge eating events, which involvethe consumption of large amounts of food in a discrete period of time. Ghrelin is theonly peptide hormone known to increasefood intake, and its receptor (GHSR) is aGproteincoupled receptor capable ofsignal in a ghrelin independent manner. The central distribution of GHSR indicates that ghrelin system regulates bothhomeostatic and hedonic aspects offeeding. Using a simple model of bingeeating, in which ad libitum fed mice areexposed to high fat diet (HFD) 4consecutive days for 2 h/day, we have shown that mice develop a HFD intakeescalation over the successive events thatinvolve the activation of the mesolimbicsystem and ghrelin signaling. Here, we tested if ghrelin evoked GHSR signaling isrequired for the HFD intake escalationand we found that the pharmacologicblockage of ghrelin signaling failed toaffect HFD intake escalation.Interestingly, mice eating HFD 2 h/day for4 successive days display an increase inGHSR levels in the ventral tegmental area(VTA), as well as an increase in cFoslevels in the dopaminergic neurons of theVTA and in the nucleus accumbens.Unexpectedly, we found that mice withGHSR expression limited to thedopaminergic neurons failed to show HFDintake escalation. Thus, we conclude thatfood intake escalation in mice dailyexposed to HFD involves ghrelinindependentGHSR signaling in a subsetof neurons different from thedopaminergic neurons of the VTA.