IGF-1 LR3 primarily exerts its effects through high-affinity binding to the IGF-1 receptor (IGF-1R), activating the insulin receptor substrate (IRS) signaling pathway, which subsequently stimulates the phosphoinositide 3-kinase (PI3K)/Akt pathway and the mitogen-activated protein kinase (MAPK) pathway. This activation promotes cellular processes such as proliferation, differentiation, and survival, particularly in fetal tissues, including cardiomyocytes and peripheral nerves. However, the complete mechanism of action, especially regarding its effects on insulin secretion and amino acid metabolism, remains not fully understood.