Highlights
- •Chronic hepatitis C is associated with metabolic disturbances.
- •Chronic hepatitis C patients have increased circulating adiponectin.
- •The association is independent of the presence of severe liver fibrosis.
- •Hyper-adiponectinemia is relatively more marked in males.
Abstract
Background
Increased levels of adiponectin, a major adipokine with insulin sensitizing properties
showing a strong sexual dimorphism, have been reported in individuals with chronic
HCV infection (CHC), but data are limited by small samples and lack of control for
the genetic background and hepatic fibrosis. The aim of this study was to compare
adiponectin levels between CHC patients and accurately matched controls.
Methods
We considered 184 CHC patients, matched (1:1) for age, gender, body mass index, and
Adiponectin genotype (ADIPOQ) with healthy individuals. To control for the severity of liver disease, a second
control group consisting of 95 patients with histological nonalcoholic fatty liver
disease (NAFLD) further matched (1:1) for severe fibrosis was exploited. ADIPOQ genotype was evaluated by Taqman assays, serum adiponectin measured by ELISA.
Results
Serum adiponectin was higher in CHC patients than in healthy individuals (9.0 ± 5.0 μg/ml vs. 7.3 ± 4.0 μg/ml; p = 0.001; adjusted estimate +1.8, 1.7–2.9; p = 0.001), and than in NAFLD patients (8.3 ± 4.5 μg/ml vs. 6.0 ± 4.2 μg/ml; p < 0.001; adjusted estimate +0.8, 0.2–1.4, p = 0.006). After stratification for sex, serum adiponectin was higher in males with CHC
than in healthy individuals and NAFLD patients (p < 0.005 for both), whereas the difference was not significant in females.
Conclusions
CHC is associated with increased serum adiponectin independently of age, body mass,
diabetes, ADIPOQ genotype, and of severe liver fibrosis, particularly in men.
Abbreviations:
HCV (hepatitis C virus), CHC (chronic HCV hepatitis), IR (insulin resistance), T2DM (type 2 diabetes mellitus), NAFLD (nonalcoholic fatty liver disease), ADIPOQ (adiponectin gene), BMI (body mass index), AST (aspartate aminotransferases), ALT (alanine aminotransferases), GGT (gamma-glutamyl-transferases)Keywords
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Article info
Publication history
Published online: August 17, 2015
Accepted:
August 3,
2015
Received in revised form:
May 4,
2015
Received:
December 23,
2014
Identification
Copyright
© 2015 European Federation of Internal Medicine. Published by Elsevier Inc. All rights reserved.