Background: Hepatitis C virus (HCV) infection is an important risk factor for insulin resistance (IR). IR, through different mechanisms, plays a role in the development of steatosis and its progression to steatohepatitis, cirrhosis and even hepatocellular carcino­ma (HCC). In addition, IR has a role in impairing tumor necrosis factor (TNF) signaling cascade, which in turn blocks signal transducer and activator of transcription-1 (STAT-1) translocation and interferon stimu­lated genes production avoiding the antiviral effect of interferon Objective: Evaluation of the prevalence of insulin resistance among chronic hepatitis C patients, and the impact of insulin resistance and serum zinc (Zn) on sustained virological response in non-diabetic, non-cirrhotic patients with chronic hepatitis C receiving combined pegylated Interferon and ribavirin therapy. Patients and Methods: This was an observational and cross-sectional study with a prospective inclusion of data that was conducted in Tropical Medicine Department, Al-Azhar University Hospitals and Gastroenterology and Hepatology Departments, Police Forces Hospitals, during the period between 2013 and 2015.There were 205 chronic hepatitis C patients who fulfilled the inclusion criteria and index of insulin resistance measured by using homeostasis model assessment of insulin resistance (HOMA-IR) which was calculated by the formula: Fasting glucose (mg/dl) x fasting insulin (µU/ml) / 405. Results: HOMA-IR among chronic hepatitis C patients was 53.2%. There were significant correlations between HOMA-IR and sustained virological response (SVR) achieved by pegylated interferon/ribavirin combination therapy. Patients with IR were more likely to have steatosis, higher grades of fibrosis  and periportal necroinflamatory activity. Conclusion: Serum zinc (Zn) has no impact on sustained virological response. The sustained virological response (SVR) rate in non insulin-resistant patients was better than in insulin-resistant patients after treatment using pegylated interferon/ribavirin combination therapy. Insulin-resistant patients had higher levels of HCV-induced liver fibrosis, steatosis and necroinflamatory activity, compared with patients without insulin resistance.