The American journal of gastroenterology · 2009
Insulin resistance in chronic hepatitis B virus infection.
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Kumar Manoj, Choudhury Ajay, Manglik Nitin, Hissar Syed, Rastogi Archana, Sakhuja Puja, Sarin Shiv K
Аннотация
OBJECTIVES: 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.
METHODS: 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).
RESULTS: 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.
CONCLUSIONS: IR in CHBV-infected patients is a reflection of the host metabolic profile and CHBV infection is not in itself correlated with IR.
METHODS: 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).
RESULTS: 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.
CONCLUSIONS: IR in CHBV-infected patients is a reflection of the host metabolic profile and CHBV infection is not in itself correlated with IR.