Liver and Biliary Tract

Subject Category: Liver and Biliary Tract

Am J Gastroenterol 2009; 104:76–82; doi:10.1038/ajg.2008.9

Insulin Resistance in Chronic Hepatitis B Virus Infection

Manoj Kumar MD, DM1, Ajay Choudhury MD, DM1, Nitin Manglik MD, DM1, Syed Hissar MD1, Archana Rastogi MD2, Puja Sakhuja MD2 and Shiv K Sarin MD, DM, FNA, FNASc1

  1. 1Department of Gastroenterology, G.B. Pant Hospital, New Delhi, India
  2. 2Department of Pathology, G.B. Pant Hospital, New Delhi, India

Correspondence: Shiv K. Sarin, MD, DM, FNA, FNASc, Department of Gastroenterology, G.B. Pant Hospital, Room No. 201, Academic Block, New Delhi 110002, India. E-mail: sksarin@nda.vsnl.net.in

Received 18 April 2008; Accepted 24 July 2008.

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Abstract

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/m2) and 18 (26.1%) were obese (BMI>25 kg/m2). 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.

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