IRS1 Expression in Hepatic Tissue and Leukocytes in Chronic Hepatitis C Virus Infected Patients: A Comparative Study

Figure 1

Mechanisms of insulin resistance (adapted from Science Oxcan et al., 2004). The figure shows both normal and alternative route of entry of glucose into the cell. With the increase of nonoxidized fatty acids by the liver, there is a change in the mechanism of tyrosine phosphorylation, and the glucose route of entry into the cell is impaired. Thereafter, intracellular insulin resistance occurs because glucose cannot enter the cell. The insulin resistance is associated with reduced expression of IRS1 and IRS2. These receptors are proteins of a family of ligands and molecules that connect insulin receptors to a cascade of reactions that allow entry of glucose into the cell. FFA: free fatty acids, P-Tyr: tyrosine, PI3-K: phosphatidylinositol kinase, ER: endoplasmic reticulum, JNK: Jun N-terminal kinase, IKKβ: inhibitor of nuclear factor kappa-b kinase subunit b, PKC: protein kinase C, IRS1 and IRS2: insulin receptor substrates 1 and 2.