Prediction of Nonalcoholic Fatty Liver Disease Via a Novel Panel of Serum Adipokines

Abstract

Considering limitations of liver biopsy for diagnosis of nonalcoholic liver disease (NAFLD), biomarkers’ panels were proposed. The aims of this study were to establish models based on serum adipokines for discriminating NAFLD from healthy individuals and nonalcoholic steatohepatitis (NASH) from simple steatosis.This case-control study was conducted in patients with persistent elevated serum aminotransferase levels and fatty liver on ultrasound. Individuals with evidence of alcohol consumption, hepatotoxic medication, viral hepatitis, and known liver disease were excluded. Liver biopsy was performed in the remaining patients to distinguish NAFLD/NASH. Histologic findings were interpreted using “nonalcoholic fatty liver activity score.” Control group consisted of healthy volunteers with normal physical examination, liver function tests, and liver ultrasound. Binary logistic regression analysis was applied to ascertain the effects of independent variables on the likelihood that participants have NAFLD/NASH.Decreased serum adiponectin and elevated serum visfatin, IL-6, TNF-a were associated with an increased likelihood of exhibiting NAFLD. NAFLD discriminant score was developed as the following: [(−0.298 × adiponectin) + (0.022 × TNF-a) + (1.021 × Log visfatin) + (0.709 × Log IL-6) + 1.154]. In NAFLD discriminant score, 86.4% of original grouped cases were correctly classified. Discriminant score threshold value of (−0.29) yielded a sensitivity and specificity of 91% and 83% respectively, for discriminating NAFLD from healthy controls. Decreased serum adiponectin and elevated serum visfatin, IL-8, TNF-a were correlated with an increased probability of NASH. NASH discriminant score was proposed as the following: [(−0.091 × adiponectin) + (0.044 × TNF-a) + (1.017 × Log visfatin) + (0.028 × Log IL-8) − 1.787] In NASH model, 84% of original cases were correctly classified. Discriminant score threshold value of (−0.22) yielded a sensitivity and specificity of 90% and 66% respectively, for separating NASH from simple steatosis.New discriminant scores were introduced for differentiating NAFLD/NASH patients with a high accuracy. If verified by future studies, application of suggested models for screening of NAFLD/NASH seems reasonable.

miR33a/miR33b* and miR122 as Possible Contributors to Hepatic Lipid Metabolism in Obese Women with Nonalcoholic Fatty Liver Disease

“…ROC analysis revealed that miR122 has the potential to distinguish NASH from SS, because it predicts hepatocellular ballooning or lobular inflammation with an AUROC of 0.76. Although this predictive value is not good enough for an ideal biomarker, the ability of miR122 to predict NASH is quite similar to that of other studies [52,53,54]. However, as these authors suggested, compared to single biomarkers, the stepwise combination of different biomarkers can further improve the accuracy of diagnosing NASH.…”

Beneficial effects of diacerein on adipokines and pro-inflammatory cytokines involved in diet-induced nonalcoholic steatohepatitis in rats

“…35 With regard to visfatin, a new adipokine with proinflammatory and metabolic properties, Jamali et al demonstrated the increased probability of NASH presence with decreased serum adiponectin and elevated levels of circulating visfatin, and TNF-α. 4 In the present research, serum visfatin levels were significantly increased in NASH rats that is in line with previous studies. 36,37 Likewise, serum visfatin was correlated with systemic insulin resistance and development of metabolic syndrome.…”

“…3 It has been suggested that the development of steatohepatitis is a consequence of the balance between pro and anti-inflammatory effects of adipokines (e.g., adiponectin, resistin, visfatin and leptin). 4 Proinflammatory cytokines such as interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α are involved in the pathogenesis of NAFLD and its progression to NASH, through their metabolic activity. 5 Feeding rodents with an atherogenic diet, which contains high-fat components, has been shown to be a useful animal model provided us with the opportunity to access the pathophysiology of progressive NAFLD and NASH in humans.…”

Association of Circulating Adipsin, Visfatin, and Adiponectin with Nonalcoholic Fatty Liver Disease in Adults: A Case-Control Study

“…Moreover, lower serum visfatin levels were inversely associated with increased risk of NAFLD. However, some studies indicated that higher circulating visfatin levels were observed in NAFLD patients than those in controls [22,38], and similar visfatin levels were observed in SS, NASH, or NAFLD patients to those in controls [19,23]. We speculated that these inconsistent results may be due to the following several possibilities, including comorbidity in NAFLD and the drugs, various adipose mass, and unknown origins of circulating visfatin.…”