Ghrelin Signaling is Required for Escalation in High-Fat Intake during Repeated Binge Eating Episodes

VALDIVIA S; CORNEJO MP; DE FRANCESCO PN; GARCIA ROMERO G; REYNALDO M; PERELLO M

La Falda

Congreso; XXIX Congreso Anual de la Sociedad Argentina de Investigación en Neurociencia; 2014

Sociedad Argentina de Investigación en Neurociencia

Binge eating is characterized by the consumption of large amounts of food in a discrete period of time, while feeling a sense of loss of control over eating. The etiology of the human binge eating is currently unknown. Ad lib fed rodents exposed to a palatable food display events of hyperphagia, which gradually escalates over the initial accesses until it finally stabilizes. Intake escalation has been proposed to mediate the transition from a controlled to a compulsive behavior. Binge eating intake in animals with intermittent access to palatable foods involves neuronal circuits regulating hedonic eating. These neuronal circuits include the dopaminergic pathways emanating from the ventral tegmental area (VTA), which project to the nucleus accumbens (Acc) among other brain areas, and the orexin neurons of the lateral hypothalamic area (LHA), which project to the VTA and are a link between homeostatic and hedonic circuits regulating food intake The molecular substrates controlling the escalation in high-fat intake in binge eating models has not been studied. Interestingly, ghrelin is recognized as the only circulating peptide hormone known to increase food intake, and several evidences show that ghrelin plays a key role as regulator of hedonic eating. However, a potential role of ghrelin signaling on binge eating models induced by intermittent access to palatable foods has not been tested.Here, we used mice to determine the neuronal brain centers activated in a binge eating model induced by intermittent access to high fat diet (HFD). We also examined the potential role of ghrelin signaling in the modulation of this behavior.