Interaction between hepatitis C virus and metabolic factors

Figure 2 Molecular mechanisms of insulin resistance in hepatitis C virus-infected hepatocytes. Hepatitis C virus (HCV) can inhibit insulin signaling directly or indirectly. GLUT: Glucose transporter; IRS: Insulin receptor substrate; SOCS: Suppressor of cytokine signaling; SREBP: Sterol regulatory element binding protein; mTOR: Mammalian target of rapamycin; MAPK: Mitogen-activated protein kinase; PTEN: Phosphatase and tensin homolog; SHIP: SH2 domain-containing inositol phosphatases; GSK3: Gen synthase kinase-3; PI3K: Phosphatidyl inositol 3-kinase; TNF: Tumor necrosis factor; ER: Endoplasmic reticulum; PP2A: Protein phosphatase 2A; PA28γ: Proteasome activator 28γ.