Hedonic and homeostatic overlap following fat ingestion

Abstract

Ingestion of fatty foods increases dopamine release in the substantia nigra, producing a positive hedonic state. Tellez et al. (2013) demonstrate that an intestinal signal generated by fat consumption, oleoylethanolamide, stimulates central dopamine activity, thus regulating the reward value of fat and establishing a link between caloric-homeostatic and hedonic-homeostatic controllers.

Figure 1

The prevailing paradigm of food intake suggests that homeostatic influences (depicted in red), including adiposity signals (i.e., leptin and insulin) and satiation signals (i.e. cholecystokinin, CCK, and glucagon-like peptide, GLP-1) provide feedback on nutrient status from the periphery to brain regions such as the arcuate nucleus (ARC) and the nucleus tractussolitarius (NTS). Non-homeostatic influences (depicted in blue) such as stress, learning and hedonics act to alter food intake independently of homeostatic influences. Oleoylethanolamide (OEA) is released from the gut in response to ingested fat and acts as a satiety signal to reduce food intake via vagal afferents to the NTS. OEA also provides hedonic feedback in a homeostatic manner by increasing dopamine reward signaling, providing a link between caloric-homeostatic and hedonic-homeostatic controllers (depicted in purple).