Metabolic disorders have been associated with CHC. Data from the 1988 to 1994 NHANES cycle showed an independent association of insulin resistance and diabetes with HCV infection. In later NHANES cycles (1998–2008), these associations were no longer found to be significant; however, the relationship may have been diluted by the increase of other risks for diabetes, most importantly the rapid increase in the prevalence of obesity [
25]. Multiple other studies have shown a causal relationship between CHC and insulin resistance, type 2 diabetes and subsequent steatosis [
26,
27]. Cheng et al. found that type 2 diabetes mellitus was seen in 28 % of CHC patients, a significantly higher prevalence compared to the study’s general population [
1]. Mehta et al. showed that CHC patients who were at high risk for diabetes were more than 11 times as likely as those without CHC to develop diabetes [
28]. Another study found that CHC is an independent predictor of diabetes [
27]. Even with adjustment for other major predisposing conditions such as older age, obesity, and smoking, CHC was associated with insulin resistance and diabetes. In a large longitudinal study that followed 4958 persons from a community-wide cohort in southern Taiwan for 7 years, it was found that CHC, coinfection with hepatitis B virus, overweight, obesity, and increasing age were significantly associated with diabetes development [
29]. Because with stratification by age and body mass index the risk ratio for diabetes in CHC participants increased when age decreased and body mass index levels increased, the researchers concluded that HCV infection is an independent predictor of diabetes, especially for CHC persons who are younger or have a higher body mass index. In patients treated with peg-IFN and ribavirin, it was found that in patients with pre-treatment insulin resistance, insulin sensitivity was improved at 12 weeks and 24 weeks, and at end of therapy (24 or 48 weeks) [
30]. The findings of both cross-sectional and longitudinal studies [
31] and a large meta-analysis [
32] have suggested a direct role of HCV in inducing derangement of glucose metabolism. The mechanism of action is thought to be secondary to an effect on glucose-insulin regulation, and lipid metabolism and synthesis [
27].