IGF-1 LR3 primarily exerts its effects through high-affinity binding to the IGF-1 receptor (IGF-1R), activating downstream signaling pathways such as the PI3K/Akt and MAPK/ERK pathways, which are crucial for cell proliferation, differentiation, and survival. This signaling promotes anabolic processes, including increased protein synthesis and cellular growth, while also influencing glucose metabolism and insulin secretion dynamics. However, the precise mechanisms by which IGF-1 LR3 modulates these pathways, particularly in the context of fetal growth and metabolic regulation, remain incompletely understood.