Gpr160 deletion alters food intake and meal patterning in mice

Cocaine- and amphetamine-regulated transcript peptide inhibits food and water intake in rodents and there is evidence that the peptide interacts with the previously orphaned G protein-coupled receptor G protein-coupled receptor (GPR160). In addition, the peptide transmits pain signals in spinal cord and loss of Gpr160 expression blocks spinal nerve injury pain perception. With the same animal model as that used to demonstrate the necessity of Gpr160 expression for pain perception, we examined food and water intakes under ad libitum conditions and following acute stress. We report that total daily food and water intakes in knockout animals do not significantly differ from those in Gpr160-expressing controls, but meal patterning is altered. On the other hand, food intake following an acute stress is altered. We conclude that in mice activation of GPR160 is not essential for unstimulated food and water ingestion, but that loss of receptor expression is sufficient to change the patterning of ingestive behavior.NEW & NOTEWORTHY Cocaine- and amphetamine-regulated transcript peptide (CARTp) acts via a G protein-coupled receptor (GPR160) to induce pain and inhibit feeding. GPR160 deletion prevents the perception of neuropathic pain and alters basal and stress-induced food intake. Although GPr160 is necessary for the sensation of painful stimuli, it appears to only affect meal patterning, but not total food intake. Antagonists of GPR160 may be useful for pain management without deleterious effects on daily food intake.