Interaction between hepatitis C virus and metabolic factors

Figure 1 Overview of insulin signaling. Insulin binding promotes receptor autophosphorylation and subsequent tyrosine phosphorylation of insulin receptor substrates, which initiate a cascade of multifaceted metabolic actions. GLUT: Glucose transporter; IRS: Insulin receptor substrate; SOCS: Suppressor of cytokine signaling; aPKC: Atypical protein kinase; SREBP: Sterol regulatory element binding protein; mTOR: Mammalian target of rapamycin; MAPK: Mitogen-activated protein kinase; PTEN: Phosphatase and tensin homolog; GSK3: Gen synthase kinase-3; SHIP: SH2 domain-containing inositol phosphatases.