IGF-1 originally called somatomedin C is a 70-amino acid hormone with homology to IGF-2 and proinsulin. IGF-1 acts as an endocrine, paracrine, and autocrine hormone and is known as a mediator of prenatal and postnatal growth. IGF-1 is mainly synthesized in the liver and regulated by growth hormones (GH) in peripheral tissues such as muscle, cartilage, bone, kidney, nerves, skin, lungs, and the liver itself. The synthesized IGF-1 binds to IGF-1 binding proteins (IGFBPs) with high affinity, IGFBPs regulates the interactions of IGF-1 and its receptor (IGF-1R)¹.

Binding of IGF-1 to his receptor results in autophosphorylation of the receptor leading to activation of the insulin receptor substrate 1 (IRS1) protein. The activated receptor contains several phosphotyrosine sites that serve as docking sites for many signaling proteins. The association of these proteins together start a complex signaling pathway including the canonical PI3-kinase and mitogen-activated protein (MAP) kinase pathways².

The IGF-1 signaling pathway is a major regulator of the aging process, from rodents to humans³. IGF-1 deficiency follows an autosomal mode of transmission and different mutations can lead to either IGF-1 deletion or low levels of circulation IGF-1. Studies demonstrate IGF-1 deficit can lead to deregulated lipid metabolism, cardiovascular disease (CVD), diabetes, and altered metabolic profile of diabetic patients⁴.