Deletion of Gpr160 alters food intake and meal organization in mice, suggesting G protein-coupled receptor's role in behavior.
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 GPR160. In addition, the peptide transmits pain signals in spinal cord and loss of Gpr160 expression blocks spinal nerve injury pain perception. Using the same animal model as that employed 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.
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Bocke et al. (2025) studied this question.
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