Insulin resistance, adipokine profile and hepatic expression of SOCS-3 gene in chronic hepatitis C

World J Gastroenterol. 2014 Aug 14;20(30):10449-56. doi: 10.3748/wjg.v20.i30.10449.

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. © 2014 Baishideng Publishing Group Inc. All rights reserved.

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

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipokines / blood*
  • Adult
  • Biomarkers / blood
  • Biopsy
  • Case-Control Studies
  • Enzyme-Linked Immunosorbent Assay
  • Fatty Liver / blood
  • Fatty Liver / genetics
  • Fatty Liver / physiopathology
  • Fatty Liver / virology
  • Female
  • Genotype
  • Hepacivirus / genetics
  • Hepacivirus / pathogenicity
  • Hepatitis C, Chronic / blood*
  • Hepatitis C, Chronic / complications
  • Hepatitis C, Chronic / diagnosis
  • Hepatitis C, Chronic / genetics
  • Hepatitis C, Chronic / physiopathology
  • Humans
  • Inflammation Mediators / blood
  • Insulin Resistance*
  • Interferons
  • Interleukins / genetics
  • Liver / chemistry*
  • Liver / pathology
  • Liver / virology
  • Liver Cirrhosis / blood
  • Liver Cirrhosis / genetics
  • Liver Cirrhosis / physiopathology
  • Liver Cirrhosis / virology
  • Male
  • Middle Aged
  • Polymorphism, Single Nucleotide
  • RNA, Messenger / analysis
  • Reverse Transcriptase Polymerase Chain Reaction
  • Risk Factors
  • Suppressor of Cytokine Signaling 3 Protein
  • Suppressor of Cytokine Signaling Proteins / genetics*
  • Young Adult

Substances

  • Adipokines
  • Biomarkers
  • interferon-lambda, human
  • Inflammation Mediators
  • Interleukins
  • RNA, Messenger
  • SOCS3 protein, human
  • Suppressor of Cytokine Signaling 3 Protein
  • Suppressor of Cytokine Signaling Proteins
  • Interferons