Alteration of Peripheral Resistin and the Severity of Acute Pancreatitis: A Meta-Analysis

Abstract

IntroductionResistin is a small secretory adipokine which is implicated to obesity and associated diseases. Recently, plenty of research papers have been conducted to explore the association between peripheral resistin and the severity of acute pancreatitis (AP). However, the results were controversial. In this study, we aimed to confirm the effect of peripheral resistin and the development of acute pancreatitis.MethodsA comprehensive online search was performed using the PubMed, Embase, Web of Science, CNKI, and Wanfang databases up through January 20, 2022. The retrieved records and their references were screened to identify additional studies. Data were extracted to calculate the pooled Hedges' g and its 95% CI, which were selected to assess peripheral resistin levels and the severity of acute pancreatitis. Subgroup analyses, sensitivity analyses, meta-regression, and publication bias tests were also undertaken based on obtained information.ResultsA total of eleven studies with 892 acute pancreatitis patients were enrolled in the study. Peripheral resistin levels were significantly increased in severe acute pancreatitis compared with mild acute pancreatitis (Hedges' g = 2.092, 95% CI: 0.994–3.190, P < 0.001). Subgroup analyses based on sample types and ethnicity also showed similar results. A single study did not affect our results, which was verified by sensitivity analysis. Meta-regression analyses revealed that age, gender of the included subjects, sample size, and publication year did not moderate effects on the present results.ConclusionIn our study, peripheral resistin levels were significantly elevated in patients with severe AP compared with patients with mild AP. Abnormal resistin levels may provide us some new insights in predicting the severity of AP.

Identification of Key Genes and Underlying Mechanisms in Cystic Fibrosis and its Associated Complications Based on Bioinformatics Analysis of Next Generation Sequencing Data Analysis

“…Accumulating evidence has demonstrated that MMP9 [116], S100A12 [117], HP (haptoglobin) [118], TLR5 [119], NRG1 [120], PLAU (plasminogen activator, urokinase) [121], SLC11A1 [122], AQP9 [123], CHIT1 [124], TLR4 [125], SLC26A8 [126], CTSD (cathepsin D) [127], SERPINB1 [128], FASLG (Fas ligand) [129], SLC4A4 [130], AQP3 [131] and IRF8 [132] appears to be constitutively associated with CF . MMP9 [133], S100A12 [134], SOCS3 [135], MMP8 [136], CRISP3 [137], S100A9 [138], RETN (resistin) [139], IL1RN [140], TLR4 [141], GGT1 [142], CTSD (cathepsin D) [143], FASLG (Fas ligand) [144], CCR4 [145], FCRL3 [146] and ABCF1 [147] were revealed and regarded as diagnostic biomarker in pancreatitis. Accumulating evidence shows that MMP9 [133], S100A12 [148], HP (haptoglobin) [149], OSM (oncostatin M) [150], PRDM5 [151], TSPO (translocator protein) [152], IL18RAP [153], ADAMDEC1 [154], IL1RN [155], SCN9A [156], FADS2 [157], NCF4 [158], SERPINB1 [159], TNFRSF13B [160], IL2RB [161], DLG5 [162], FASLG (Fas ligand) [163], GPR68 [164], IL2RA [161], TCF4 [165], TAGAP (T cell activation RhoGTPase activating protein) [166], ABCB1 [167], FCRL3 [168], ITGB7 [169], PTGER4 [170] and TRAF3IP2 [171] are altered expression in gastrointestinal complications.…”

Acute pancreatitis: pathogenesis and emerging therapies

“…A meta-analysis of 11 studies involving 892 AP patients found that circulating resistin levels were significantly higher in patients with SAP than those with mild AP, suggesting that elevated resistin levels may predict AP. [77] Activin A, a member of the TGF-β superfamily, has recently emerged as a significant potential mediator of inflammation in AP. Activin A is released into the bloodstream during inflammatory events and modulates inflammatory responses.…”

“…A meta-analysis of 11 studies involving 892 AP patients found that circulating resistin levels were significantly higher in patients with SAP than those with mild AP, suggesting that elevated resistin levels may predict AP. [77]…”

Predictive value of adipokines for the severity of acute pancreatitis: a meta-analysis

“…Visfatin promotes the release of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α from peripheral monocytes [17][18][19] Despite many studies having explored the relationship between adipokines and SAP, the findings have been inconsistent. Furthermore, although a meta-analysis of the relationship between adipokines and SAP has recently been published [20], it only statistically examined the relationship between resistin and SAP, failing to address the correlation between other adipokines and SAP.…”