2021
DOI: 10.14218/jcth.2021.00018
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Serum Resistin Levels in Adult Patients with Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-analysis

Abstract: Newcastle-Ottawa Quality Assessment Scale:Case-Control Studies• Selection (4)• Comparability (1)• Exposure (3)-A study can be awarded a maximum of one star for each numbered item within the Selection and Exposure categories.A maximum of two stars can be given for Comparability

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Cited by 12 publications
(17 citation statements)
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“…Resistin reduces the number of mitochondria and increases fat accumulation. Its expression was shown to be higher in patients with NASH compared to simple steatosis and control subjects [ 65 , 70 ]. It is produced by adipose tissue macrophages and monocytes, induces IR, angiogenesis, and smooth muscle cell proliferation [ 71 ].…”
Section: Organokinesmentioning
confidence: 99%
“…Resistin reduces the number of mitochondria and increases fat accumulation. Its expression was shown to be higher in patients with NASH compared to simple steatosis and control subjects [ 65 , 70 ]. It is produced by adipose tissue macrophages and monocytes, induces IR, angiogenesis, and smooth muscle cell proliferation [ 71 ].…”
Section: Organokinesmentioning
confidence: 99%
“…Similarly, most adipokines and hepatokines display contradictory roles regarding the progression of NAFLD ( 27 , 167 ) ( Tables 3 and 4 ). In this regard, resistin, a pro-inflammatory adipokine acting via NF-κB/TLR4 mediated pathway and overexpressed in NASH ( 98 ) can still promote an anti-inflammatory response in the presence of LPS ( 100 , 137 , 168 ). Fetuin A, a hepatokine which induces MetS has been associated with a controversial role in liver fibrosis ( 119 , 120 ) similar to chemerin in liver inflammation ( 86 , 124 ).…”
Section: Hepatokine/adipokine Axis In Nafld Pathogenesismentioning
confidence: 99%
“…9 This definition, despite initial doubts, may be of better clinical utility, as demonstrated in recent cohort studies. 10 In the present issue of Journal of Clinical and Translational Hepatology, Han and colleagues 11 performed a thorough and methodologically rigorous meta-analysis assessing the potential applicability of serum resistin, a pro-inflammatory adipokine, as a biomarker of NAFLD at its entire spectrum. The authors initially demonstrated that subjects with NAFLD have significantly higher serum resistin levels compared to controls [standardized mean difference (SMD) = 0.522, 95% confidence interval (CI): 0.004 to 1.040, I 2 =95.9%] and subjects with NASH have lower serum resistin levels than the healthy controls (SMD = −0.44, 95% CI: −0.83 to −0.55, I 2 =74.5%), while no significant difference was identified for patients with NAFL compared to controls and patients with NAFL compared to those with NASH.…”
Section: Dimitrios Patoulias *mentioning
confidence: 99%
“…The authors initially demonstrated that subjects with NAFLD have significantly higher serum resistin levels compared to controls [standardized mean difference (SMD) = 0.522, 95% confidence interval (CI): 0.004 to 1.040, I 2 =95.9%] and subjects with NASH have lower serum resistin levels than the healthy controls (SMD = −0.44, 95% CI: −0.83 to −0.55, I 2 =74.5%), while no significant difference was identified for patients with NAFL compared to controls and patients with NAFL compared to those with NASH. Based on the contradictory results, Han et al 11 performed a meticulous sensitivity analysis, documenting that patients with NASH have lower resistin levels compared to healthy controls, whereas no significant difference between NAFL patients versus controls and NAFL versus NASH patients exists. Additionally, their thorough meta-regression analysis failed to identify any significant source of the high observed heterogeneity for the generated results.…”
Section: Dimitrios Patoulias *mentioning
confidence: 99%
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