Correlation of visfatin level with non-alcoholic fatty liver in metabolic syndrome

Mousavi, Zohreh; Ganji, Azita; Tehrani, Donya Farrokh; Bahari, Ali; Esmaeilzadeh, Abbas; Delghandi, Mehdi

doi:10.18869/mjiri.31.28

Cited by 12 publications

(18 citation statements)

References 17 publications

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“…We previously evaluated the effects of visfatin on inflammation and insulin resistance in HepG2 cells and the molecular mechanisms involved [32]. In addition, several studies have reported an association between the circulating visfatin level and NAFLD [33,34], and some studies have described increases in liver visfatin expression levels in NAFLD [35,36]. In our results, visfatin induced CCL20 expression and secretion in macrophages.…”

Section: Discussionsupporting

confidence: 65%

CCL20 induced by visfatin in macrophages via the NF-κB and MKK3/6-p38 signaling pathways contributes to hepatic stellate cell activation

et al. 2020

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Chemokines interact with hepatic resident cells during inflammation and fibrosis. CC chemokine ligand (CCL) 20 has been reported to be important in inflammation and fibrosis in the liver. We hypothesized that visfatin, an adipocytokine, could play a role in hepatic fibrosis via CCL20. We investigated the effect of visfatin on CCL20 in THP-1 human promonocytic cells and examined the molecular mechanisms involved. Following treatment of THP-1 cells with visfatin, CCL20 expression and secretion were assessed. We assessed the intracellular signaling molecules IKK/NF-κB, JAK2/STAT3, MAPKs, and MKK3/6 by western blotting. We treated THP-1 cells with visfatin and signaling inhibitors, and examined CCL20 mRNA and protein levels. To investigate the effect of visfatin-induced CCL20 expression in hepatic stellate cells (HSCs), LX-2 cells were co-cultured with the culture supernatant of THP-1 cells with or without anti-CCL20 neutralizing antibodies, and fibrosis markers were examined by RT-PCR and immunoblotting. In THP-1 cells, visfatin increased the CCL20 mRNA and protein levels. visfatin increased the activities of the NF-κB, p38, and MLK3/6 signaling pathways but not those of the JAK2/STAT3 and ERK pathways. Visfatin treatment together with an NF-κB, p38, or MLK3 inhibitor reduced the mRNA and protein levels of CCL20. The visfatin-induced CCL20 increased the expression of fibrosis markers and CCR6 in HSCs. Following neutralization of CCL20, the levels of fibrosis markers and CCR6 were decreased. Visfatin increases the expression of CCL20 via the NF-κB and MKK3/6-p38 signaling pathways in macrophages, and visfatin-induced CCL20 expression promotes the fibrosis markers in HSCs.

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Section: Discussionsupporting

confidence: 65%

CCL20 induced by visfatin in macrophages via the NF-κB and MKK3/6-p38 signaling pathways contributes to hepatic stellate cell activation

et al. 2020

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“…Several adipocytokines have been suggested to play important roles in pathogenesis [10]. The role of visfatin in NAFLD has been evaluated, but the results were inconsistent [11–13], and it remains unclear whether visfatin contributes to hepatic insulin resistance and inflammation. Moreover, the effects of visfatin as an adipocytokine in hepatocytes have rarely been explored.…”

Section: Introductionmentioning

confidence: 99%

Visfatin Induces Inflammation and Insulin Resistance via the NF-κB and STAT3 Signaling Pathways in Hepatocytes

Heo

Choi

Jeon

et al. 2019

Journal of Diabetes Research

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Background. It has been suggested that visfatin, which is an adipocytokine, exhibits proinflammatory properties and is associated with insulin resistance. Insulin resistance and inflammation are the principal pathogeneses of nonalcoholic fatty liver disease (NAFLD), but the relationship, if any, between visfatin and NAFLD remains unclear. Here, we evaluated the effects of visfatin on hepatic inflammation and insulin resistance in HepG2 cells and examined the molecular mechanisms involved. Methods. After treatment with visfatin, the inflammatory cytokines IL-6, TNF-α, and IL-1β were assessed by real-time polymerase chain reaction (RT-PCR) and immunocytochemical staining in HepG2 cells. To investigate the effects of visfatin on insulin resistance, we evaluated insulin-signaling pathways, such as IR, IRS-1, GSK, and AKT using immunoblotting. We assessed the intracellular signaling molecules including STAT3, NF-κB, IKK, p38, JNK, and ERK by western blotting. We treated HepG2 cells with both visfatin and either AG490 (a JAK2 inhibitor) or Bay 7082 (an NF-κB inhibitor); we examined proinflammatory cytokine mRNA levels using RT-PCR and insulin signaling using western blotting. Results. In HepG2 cells, visfatin significantly increased the levels of proinflammatory cytokines, reduced the levels of proteins (e.g., phospho-IR, phospho-IRS-1 (Tyr612), phospho-AKT, and phospho-GSK-3α/β) involved in insulin signaling, and increased IRS-1 S307 phosphorylation compared to controls. Interestingly, visfatin increased the activities of the JAK2/STAT3 and IKK/NF-κB signaling pathways but not those of the JNK, p38, and ERK pathways. Visfatin-induced inflammation and insulin resistance were regulated by JAK2/STAT3 and IKK/NF-κB signaling; together with AG490 or Bay 7082, visfatin significantly reduced mRNA levels of IL-6, TNF-α and IL-1β and rescued insulin signaling. Conclusion. Visfatin induced proinflammatory cytokine production and inhibited insulin signaling via the STAT3 and NF-κB pathways in HepG2 cells.

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“…Upon reviewing the references of included studies manually, one relevant article was recognized and included in our analysis. The total number of articles included in the qualitative synthesis was 21 articles, out of which 14 articles were included in the quantitative synthesis [ 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 ].…”

Section: Resultsmentioning

confidence: 99%

Serum Visfatin Levels in Nonalcoholic Fatty Liver Disease and Liver Fibrosis: Systematic Review and Meta-Analysis

Ismaiel

Leucuţa

Popa

et al. 2021

JCM

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(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 1,923 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.

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Correlation of visfatin level with non-alcoholic fatty liver in metabolic syndrome

Cited by 12 publications

References 17 publications

CCL20 induced by visfatin in macrophages via the NF-κB and MKK3/6-p38 signaling pathways contributes to hepatic stellate cell activation

CCL20 induced by visfatin in macrophages via the NF-κB and MKK3/6-p38 signaling pathways contributes to hepatic stellate cell activation

Visfatin Induces Inflammation and Insulin Resistance via the NF-κB and STAT3 Signaling Pathways in Hepatocytes

Serum Visfatin Levels in Nonalcoholic Fatty Liver Disease and Liver Fibrosis: Systematic Review and Meta-Analysis

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