Mechanistically, autocrine IGF-2 promotes self-activation by binding to the IGF-1 receptor (IGF-1R) on CAFs and activating PI3K/AKT signaling, followed by the secretion of various chemokines and cytokines (CCL5 and CXCL12) by CAFs to influence the infiltration of T cell
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This phenomenon is independent of DPP-IV, the GLP-1 receptor, or the PYY related peptide NPY
They enhance glucose-dependent insulin secretion, suppress glucagon release, delay gastric emptying, and reduce appetite, thereby contributing to glucose homeostasis and body weight regulation (29, 30)
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