INS and Insulin resistance: The heightened risk of NODAT associated with HCV infection may be attributed to multiple factors, such as the direct replication of the HCV virus in pancreatic islet β-cells leading to dysfunction and autoimmune destruction, causing inadequate insulin synthesis and secretion; direct damage to liver cells by HCV, resulting in impaired insulin utilization and insulin resistance; and the potential impact of HCV on the synthesis of insulin-related proteins through the mediation of the insulin signaling pathway, ultimately affecting insulin secretion [29].