ArticleClinical and experimental hepatology2019
Visfatin serum concentration and hepatic mRNA expression in chronic hepatitis C.
Article in Clinical and experimental hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Immunohistochemical identification and assessment of the location of leptin, visfatin and chemerin in the liver of men with different body mass index.BMC gastroenterology · 2022Article
- Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aim of the studyChronic 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
methodsIn 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/m
resultsSerum visfatin levels were significantly higher in CHC patients compared to controls (22.7 ±5.7 vs. 17.8 ±1.5 ng/ml,
conclusionsSerum 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.
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