Insulin Resistance in Chronic Hepatitis B Virus Infection

• Published in: The American journal of gastroenterology Vol. 104; no. 1; pp. 76 - 82
• Main Authors: KUMAR, Manoj, CHOUDHURY, Ajay, MANGLIK, Nitin, HISSAR, Syed, RASTOGI, Archana, SAKHUJA, Puja, SARIN, Shiv K
• Format: Journal Article
• Language: English
• Published: Basingstoke Nature Publishing Group 01.01.2009; Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins
• Subjects: Adult; Biological and medical sciences; Blood Glucose - analysis; Body Mass Index; C-Peptide - blood; Female; Gastroenterology; Gastroenterology. Liver. Pancreas. Abdomen; Glucose Tolerance Test; Hepatitis B; Hepatitis C, Chronic - metabolism; Hepatitis C, Chronic - pathology; Human viral diseases; Humans; Infectious diseases; Insulin - blood; Insulin Resistance; Insulin-Secreting Cells - metabolism; Liver - pathology; Male; Medical sciences; Viral diseases; Viral hepatitis; Endocrinopathy; Infection; Viral hepatitis B; Target tissue resistance; Viral disease; Gastroenterology; Metabolic diseases; Digestive diseases; Hepatic disease; Insulin resistance
• ISSN: 0002-9270; 1572-0241
• DOI: 10.1038/ajg.2008.9

Chronic hepatitis C virus infection is associated with insulin resistance (IR), and both host and viral factors are important in its development. The association and the predictors of IR in chronic hepatitis B virus (CHBV) infection remain unclear. A total of 69 CHBV-infected subjects were examined to study the relationship between histological findings and anthropometric and biochemical data, including IR determined by the homeostasis model assessment (HOMA-IR). To assess the influence of CHBV infection on IR independent of any effect of hepatic fibrosis, overweight, or sex we also compared fasting serum insulin, C-peptide, HOMA-IR, HOMA-beta (measure of beta-cell function) and C-peptide-insulin ratio (to distinguish impaired insulin degradation (low ratio) from insulin hypersecretion (normal ratio)) levels between the subset of 14 male normal weight (body mass index, BMI<23) CHBV patients with stage 0 or 1 hepatic fibrosis and 50 male normal weight healthy controls matched by age and anthropometry (BMI and waist circumference). A total of 31 (44.9%) CHBV-infected patients were overweight (BMI>23 kg/m(2)) and 18 (26.1%) were obese (BMI>25 kg/m(2)). IR was seen in 34 (49.3%) patients. BMI (Spearman's coefficient=-0.436; P<0.001) and serum triglyceride levels (Spearman's coefficient=-0.307; P=0.010) were univariate predictors of IR. In multiple linear regression analysis, only BMI (P<0.001) was an independent predictor of HOMA-IR. The subgroup of CHBV-infected patients and the controls had comparable levels of all markers of IR, including fasting glucose, insulin, C-peptide, and HOMA-IR. IR in CHBV-infected patients is a reflection of the host metabolic profile and CHBV infection is not in itself correlated with IR.