Gut-brain crosstalk regulates craving for fatty food

Core Tip

Core tip: The mechanisms underlying a massive and sustained body weight loss after gastric bypass surgery remain poorly understood. Hankir et al describe how a fat-satiety signaling pathway that was greatly blunted in obese rats could be restored by Roux-en-Y gastric bypass (RYGB) surgery. The authors have demonstrated that RYGB rats on high fat diet (HFD) elicited an increased production of oleoylethanolamide (OEA) and activation of PPARα that led to a surge in dopamine release and activation of D1 in the dorsal striatum. The enhanced dopamine neurotransmission evoked by OEA was obligatorily dependent on intact vagus nerve that had no effect on the production of OEA in the small intestine. The heightened dopamine neurotransmission in the midbrain of RYGB rats was linked to their decreased preference for HFD. These elegant studies have provided a compelling mechanism by which RYGB surgery led to altered gut-brain communication to modify the reward circuitry involved in food preference and obesity. These observations have important clinical implications for the amelioration obesity and its pathological consequences.