Abstract

(1) Background: Recently, adipokines, including visfatin, have been studied in nonalcoholic fatty liver disease (NAFLD). Several studies evaluated visfatin levels in NAFLD, the presence and severity of hepatic steatosis, liver fibrosis, lobar inflammation, nonalcoholic steatohepatitis (NASH), and gender differences. However, inconclusive results have been reported. Accordingly, we performed a systematic review and meta-analysis, aiming to address these gaps in evidence. (2) Methods: We performed a systematic electronic search on PubMed, EMBASE, and Cochrane Library using predefined keywords. Diagnosis of NAFLD by liver biopsy or imagistic investigations was accepted. Full articles satisfying our inclusion and exclusion criteria were included. NHLBI quality assessment tools were used to evaluate included studies. The principal summary outcome was the mean difference in visfatin levels. (3) Results: There were 21 studies involving 1923 individuals included in our qualitative assessment, while 14 studies were included in the quantitative assessment. No statistical significance was found assessing visfatin levels in NAFLD [3.361 (95% CI −0.175–6.897)], simple steatosis [7.523 (95% CI −16.221–31.267)], hepatic steatosis severity [−0.279 (95% CI −1.843–1.285)], liver fibrosis [4.133 (95% CI −3.176–11.443)], lobar inflammation [0.358 (95% CI −1.470–2.185)], NASH [−2.038 (95% CI −6.839–2.763)], and gender [(95% CI −0.554–0.556)]. (4) Conclusions: In conclusion, visfatin levels are not associated with NAFLD, presence or severity of hepatic steatosis, liver fibrosis, lobar inflammation, NASH, and gender. However, due to the limited methodological quality of the included studies, results should be interpreted with caution.

Highlights

  • Nonalcoholic fatty liver disease (NAFLD) is primarily a liver pathology associated with structural and functional liver modifications, increased liver-related morbidity and mortality due to possible progression to cirrhosis, liver failure, and hepatocellular carcinoma, as well as several extrahepatic manifestations [1,2,3,4]

  • (4) Conclusions: In conclusion, visfatin levels are not associated with nonalcoholic fatty liver disease (NAFLD), presence or severity of hepatic steatosis, liver fibrosis, lobar inflammation, nonalcoholic steatohepatitis (NASH), and gender

  • We aimed to review all the current evidence published on PubMed, EMBASE, and Cochrane Library reporting observational studies assessing the role of visfatin in NAFLD, the presence and severity of hepatic steatosis, liver fibrosis, lobar inflammation, and NASH, as well as gender differences

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Summary

Introduction

Nonalcoholic fatty liver disease (NAFLD) is primarily a liver pathology associated with structural and functional liver modifications, increased liver-related morbidity and mortality due to possible progression to cirrhosis, liver failure, and hepatocellular carcinoma, as well as several extrahepatic manifestations [1,2,3,4]. The worldwide prevalence of associated metabolic diseases such as NAFLD, type 2 diabetes mellitus, dyslipidemia, and obesity has dramatically increased over the last decades [8]. The development and progression of NAFLD are based on a complex and multifactorial mechanism, explained by a recent hypothesis known as the “multiple-hit model” that has been more widely accepted, describing a prominent metabolic dysfunction due to several genetic and environmental interactions, in addition to changes in crosstalk between several organs and tissues such as adipose tissue, liver, pancreas, and gut [9]. The pathogenic effects exerted by adipokines in NAFLD remain under investigation

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