Gpr171, a G-protein-coupled receptor, has diverse functions. It is involved in regulating food intake and metabolism as the receptor for the neuropeptide BigLEN [7]. It also has connections with pain modulation, T-cell immunity, and lipid metabolism. It is thought to be related to the P2Y family of purinergic receptors and may play a role in hematopoiesis [6].

In terms of disease-related findings, Gpr171 deficiency in mice exacerbates dextran sulfate sodium (DSS)-and CD45RBhighCD4+ T-cell-induced colitis. Mechanistically, it promotes Th17 cell differentiation and alters lipidome profile in Th17 cells via the cAMP-pCREB-FABP5 axis [1]. In cancer, Gpr171 expression enhances the proliferation and metastasis of lung cancer cells, and in breast cancer, it is associated with brain metastasis [4,5]. In pain research, activation of Gpr171 with an agonist attenuates morphine tolerance in both female and male mice in the tail-flick test, and its agonist can alleviate chronic pain in male mice but not in female mice [2,3].

In conclusion, Gpr171 is crucial in multiple biological processes. Gene knockout mouse models have revealed its role in intestinal inflammation, cancer progression, and pain modulation. These findings provide insights into potential therapeutic strategies for diseases such as inflammatory bowel disease, cancer, and chronic pain.