Research Report
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World J Gastroenterol. Aug 14, 2014; 20(30): 10449-10456
Published online Aug 14, 2014. doi: 10.3748/wjg.v20.i30.10449
Insulin resistance, adipokine profile and hepatic expression of SOCS-3 gene in chronic hepatitis C
Kamila Wójcik, Elżbieta Jabłonowska, Aleksandra Omulecka, Anna Piekarska
Kamila Wójcik, Elżbieta Jabłonowska, Anna Piekarska, Department of Infectious Diseases and Hepatology, Medical University of Lodz, 91-347 Łódź, Poland
Aleksandra Omulecka, Department of Pathology, Bieganski Hospital of Lodz, 91-347 Łódź, Poland
Author contributions: Wójcik K and Jablonowska E contributed equally to this work; Wójcik K, Jablonowska E and Piekarska A designed the research; Wójcik K, Jabłonowska E and Omulecka A performed the research; Wójcik K and Jabłonowska E analyzed the data; Wójcik K and Jabłonowska E wrote the paper.
Supported by Medical University, Lodz, Poland, No. 502-03/1-117-01/502-14-061
Correspondence to: Kamila Wójcik, MD, PhD, Department of Infectious Diseases and Hepatology, Medical University of Łódź, Kniaziewicza 1/5, 91-347 Łódź, Poland. camilaw@tlen.pl
Telephone: +48-42-2516265 Fax: +48-42-2516180
Received: October 8, 2013
Revised: May 4, 2014
Accepted: May 23, 2014
Published online: August 14, 2014
Processing time: 314 Days and 11.3 Hours
Abstract

AIM: To analyze adipokine concentrations, insulin resistance and hepatic expression of suppressor of cytokine signaling 3 (SOCS-3) in patients with chronic hepatitis C genotype 1 with normal body weight, glucose and lipid profile.

METHODS: The study group consisted of 31 patients with chronic hepatitis C and 9 healthy subjects. Total levels of adiponectin, leptin, resistin, visfatin, omentin, osteopontin and insulin were measured using an ELISA kit. The hepatic expression of SOCS-3 was determined by the use of the reverse transcription polymerase chain reaction method.

RESULTS: Homeostasis model assessment for insulin resistance (HOMA-IR) values were significantly higher in hepatitis C virus (HCV) infected patients without metabolic disorders compared to healthy controls (2.24 vs 0.59, P = 0.0003). Hepatic steatosis was observed in 32.2% of patients with HCV infection and was found in patients with increased HOMA-IR index (2.81 vs 1.99, P = 0.05) and reduced adiponectin level (5.96 vs 8.37, P = 0.04). Inflammatory activity (G ≥ 2) was related to increased osteopontin concentration (34.04 vs 23.35, P = 0.03). Advanced liver fibrosis (S ≥ 2) was associated with increased levels of omentin and osteopontin (436.94 vs 360.09, P = 0.03 and 32.84 vs 20.29, P = 0.03) and reduced resistin concentration (1.40 vs 1.74, P = 0.047). No correlations were reported between adipokine profile, HOMA-IR values and hepatic expression of the SOCS-3 gene.

CONCLUSION: We speculated that no relationship between adipokines and HOMA-IR values may indicate that HCV can induce insulin resistance itself. Some adipokines appear to be biochemical markers of steatosis, inflammation and fibrosis in patients with chronic HCV infection.

Keywords: Adipokines; Steatosis; Chronic hepatitis C; Insulin resistance; SOCS-3 gene

Core tip: To investigate the direct effect of hepatitis C virus (HCV) on insulin resistance we analyzed adipokines and homeostasis model assessment for insulin resistance (HOMA-IR) in selected chronic hepatitis C patients without metabolic disorders. In this group of patients we confirmed higher HOMA-IR values compared to healthy subjects. We speculated that no relationship between adipokines and HOMA-IR values may indicate that HCV can induce insulin resistance itself, regardless of metabolic disorders. This is the first study to determine the impact of a wide spectrum of adipokines and HOMA-IR index on histopathological changes in liver biopsy specimens and hepatic expression of suppressor of cytokine signaling 3 mRNA.