Hepatitis C virus NS5A promotes insulin resistance through IRS-1 serine phosphorylation and increased gluconeogenesis

Figure 2 Status of p-Ser³⁰⁷ insulin receptor substrate-1 and p-Ser⁴⁷³ Akt phosphorylation in hepatitis C virus infected hepatoma cells upon insulin treatment. Total cellular lysates were prepared from hepatitis C virus (HCV) infected and mock infected Huh7.5 cells that were treated or untreated with insulin (100 nmol/L). An equal amount of cellular lysates were subjected to Western blot assay using anti-p-IRS-1 Ser³⁰⁷ and anti-p-Akt Ser⁴⁷³. Cellular actin was used as a protein loading control in each lane. IRS: Insulin receptor substrate.