Search tips
Search criteria 


Logo of gutGutView this articleSubmit a manuscriptReceive email alertsContact usBMJ
Gut. 2007 August; 56(8): 1167–1168.
PMCID: PMC1955513

Links between triglyceride levels, hepatitis C virus infection and diabetes

We read the interesting article by Marzouk et al (Gut 2007;56:1105–10). The authors enrolled 765 residents in Egypt and reported prevalences of hepatitis C virus (HCV) antibody (anti‐HCV), chronic and past HCV infection of 23.5%, 14% and 8.8%, respectively. Patients with chronic HCV infection had lower triglyceride levels and those with past HCV infection had higher triglyceride levels than those never infected. With a diabetes prevalence of 5.4%, HCV infection status—but not triglyceride levels—was one of the independent factors associated with diabetes.

We have conducted a large‐scale community‐based study of 9932 residents aged 40–65 years in Kaohsiung City, Taiwan, a country endemic for hepatitis B virus (HBV) infection. The prevalences of anti‐HCV, hepatitis B surface antigen (HBsAg) and diabetes were 6.5%, 13.1% and 12.5%, respectively. In 642 anti‐HCV‐positive residents the prevalences of HCV RNA (tested using the COBAS AMPLICOR HCV test Version 2.0; Roche, Branchburg, New Jersey, USA), HBsAg and diabetes were 74.5%, 11.7% and 15%, respectively. Subjects with positive HCV RNA had significantly lower triglyceride levels (115.7 (67.1) vs 133.3 (134.3) mg/dl, p = 0.029), a significantly lower proportion of abnormal triglyceride levels ([gt-or-equal, slanted]150 mg/dl) (18.6% vs 29.3%, p = 0.004) and a higher proportion of diabetes than HCV RNA‐negative subjects (18.0% vs 6.1%, p<0.001). Clinical factors associated with diabetes and abnormal triglyceride levels by univariate analyses are shown in table 11.. Higher levels of alanine aminotransferase and triglyceride and a higher proportion of abnormal triglyceride levels and positive HCV RNA were significantly associated with diabetes (all p<0.005). A higher body mass index (BMI), higher proportions of diabetes and negative HCV RNA were significantly associated with abnormal triglyceride levels (all p<0.05). Based on multivariate analyses, the HCV RNA status and abnormal triglyceride levels were independent factors associated with diabetes, and diabetes, BMI and HCV RNA status were independent factors associated with abnormal levels of triglyceride (table 22).

Table thumbnail
Table 1 Comparison of factors in subjects with and without diabetes and subjects with and without abnormal triglyceride levels among 642 anti‐HCV‐positive subjects
Table thumbnail
Table 2 Stepwise logistic regression analysis of factors significantly associated with diabetes and abnormal triglyceride levels in 642 anti‐HCV‐positive subjects

It is noteworthy that we enrolled 642 anti‐HCV‐positive subjects in whom the HCV RNA status was determined and found an association between diabetes and abnormal levels of triglyceride which was not found by Marzouk et al in 180 subjects of known HCV RNA status. We observed significantly lower triglyceride levels and a higher prevalence of diabetes in HCV‐infected subjects compared with HCV‐cleared subjects, which might imply a direct involvement of HCV in the development of insulin resistance.1 Taken together, the significant association between HCV infection and diabetes and lower triglyceride levels in our study might strengthen the finding that HCV infection has an effect on the decrease in triglyceride levels. Whether a possible association between HCV infection and hypobetalipoproteinaemia2,3 could explain our findings needs further study. The proportion of HCV clearance was lower in our subjects from Taiwan than in those from Egypt (25.5% vs 37.2%). The relation between host or virological factors such as ethnicity or HCV genotypes (major genotype 1 and 2 in Taiwan4 and genotype 4 in Egypt) and different HCV clearance rates needs further clarification. In addition, the HBsAg status, which was not evaluated by Marzouk et al, did not appear to be associated with diabetes and abnormal triglyceride levels in this HBV endemic area.


Competing interests: None.


1. Shintani Y, Fujie H, Miyoshi H. et al Hepatitis C virus infection and diabetes: direct involvement of the virus in the development of insulin resistance. Gastroenterology 2004. 126840–848.848 [PubMed]
2. Perlemuter G, Sabile A, Letteron P. et al Hepatitis C virus core protein inhibits microsomal triglyceride transfer protein activity and very low density lipoprotein secreation: a model of viral‐related steatosis. FASEB J 2002. 16185–194.194 [PubMed]
3. Serfaty L, Andreani T, Giral P. et al Hepatitis C virus induced hypobetalipoproteinemia: a possible mechanism for steatosis in chronic hepatitis C. J Hepatol 2001. 34428–434.434 [PubMed]
4. Dai C Y, Chuang W L, Chang W Y. et al Tumor necrosis factor alpha promoter polymorphism at position −308 predicts hepatitis C virus response to combination therapy. J Infect Dis 2006. 19398–101.101 [PubMed]

Articles from Gut are provided here courtesy of BMJ Publishing Group