eISSN: 2449-8238
ISSN: 2392-1099
Clinical and Experimental Hepatology
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SCImago Journal & Country Rank
2/2019
vol. 5
 
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abstract:
Original paper

Visfatin serum concentration and hepatic mRNA expression in chronic hepatitis C

Michał Kukla
,
Marzena Zalewska-Ziob
,
Brygida Adamek
,
Janusz Kasperczyk
,
Rafał J. Bułdak
,
Tomasz Sawczyn
,
Dominika Stygar
,
Barbara Sobala-Szczygieł
,
Marta Stachowska
,
Andrzej Gabriel
,
Andrzej Wiczkowski

Clin Exp HEPATOL 2019; 5, 2: 147–154
Online publish date: 2019/05/14
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Aim of the study
Chronic hepatitis C (CHC) is a viral disease with metabolic disturbances involved in its pathogenesis. Adipokines may influence the inflammatory response and contribute to development of metabolic abnormalities in CHC. Visfatin exerts immunomodulatory and insulin-mimetic effects. The aim was to measure visfatin serum concentrations and its mRNA hepatic expression in non-obese CHC patients and to assess the relationships with metabolic and histological parameters.

Material and methods
In a group of 63 non-obese CHC patients (29 M/34 F) infected with genotype 1b aged 46.6 ±14.6 years, body mass index (BMI) 24.8 ±3.0 kg/m2, serum visfatin levels and its mRNA hepatic expression were examined and the subsequent associations with metabolic and histopathological features were assessed.

Results
Serum visfatin levels were significantly higher in CHC patients compared to controls (22.7 ±5.7 vs. 17.8 ±1.5 ng/ml, p < 0.001). There was no difference in serum visfatin and its mRNA hepatic expression regardless of sex, BMI, insulin sensitivity and lipids concentrations. There was no mutual correlation between serum visfatin and visfatin mRNA hepatic expression. Hepatic visfatin mRNA levels but not visfatin serum levels were higher in patients with steatosis (1.35 ±0.75 vs. 0.98 ±0.34, p = 0.009).

Conclusions
Serum visfatin levels may reflect its involvement in chronic inflammatory processes accompanying HCV infection. Increased visfatin mRNA hepatic expression in patients with steatosis seems to be a compensatory mechanism enabling hepatocytes to survive metabolic abnormalities resulting from virus-related lipid droplet deposition prerequisite to HCV replication.

keywords:

visfatin, adipokine, chronic hepatitis C, fibrosis, insulin resistance, steatosis, liver

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