Liver Fatty Acid-binding Protein Is A Diagnostic Marker to Detect Liver Injury Due to Chronic Hepatitis C Infection

Akbal, Erdem; Köklü, Seyfettin; Koçak, Erdem; Çakal, Başak; Güneş, Fahri; Başar, Ömer; Tuna, Yaşar; Şeneş, Mehmet

doi:10.1016/j.arcmed.2012.11.007

Cited by 35 publications

(36 citation statements)

References 31 publications

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“…Our previous studies have reported that when there was a strong correlation between Knodell score and L-FABP, there was no significant association of Knodell score with ALT or AST. Therefore, L-FABP may be considered to be superior to ALT and AST [22]. Two other studies found that L-FABP was elevated with the Pringle manoeuvre during liver surgery, whereas aminotransferases did not change significantly [26,27].…”

Section: Resultsmentioning

confidence: 95%

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Liver fatty acid-binding protein as a diagnostic marker for non-alcoholic fatty liver disease

Akbal

Koçak

Akyürek

et al. 2014

Wien Klin Wochenschr

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Section: Resultsmentioning

confidence: 95%

“…In another study, it was reported that urinary excretions of L-FABP are increased in patients with chronic hepatitis [21]. We previously reported that L-FABP levels are elevated in chronic hepatitis C (CHC) patients [22]. However, to our knowledge there has been no study investigating the relationship between L-FABP and NAFLD.…”

Section: Introductionmentioning

confidence: 93%

Liver fatty acid-binding protein as a diagnostic marker for non-alcoholic fatty liver disease

Akbal

Koçak

Akyürek

et al. 2014

Wien Klin Wochenschr

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“…Recently, the pre- dictive and prognostic value of L-FABP in liver diseases has attracted considerable attention. Numerous studies have demonstrated that L-FABP can be used as a new diagnostic biomarker for hepatic injury and impaired function of hepatocytes (53)(54)(55). However, to date, there has been no study examining the change of L-FABP expression in TB patients.…”

Section: Discussionmentioning

confidence: 99%

Liver Fatty Acid Binding Protein Deficiency Provokes Oxidative Stress, Inflammation, and Apoptosis-Mediated Hepatotoxicity Induced by Pyrazinamide in Zebrafish Larvae

Zhang

Liu

Hassan

et al. 2016

Antimicrob Agents Chemother

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g Pyrazinamide (PZA) is an essential antitubercular drug, but little is still known about its hepatotoxicity potential. This study examined the effects of PZA exposure on zebrafish (Danio rerio) larvae and the mechanisms underlying its hepatotoxicity. A transgenic line of zebrafish larvae that expressed enhanced green fluorescent protein (EGFP) in the liver was incubated with 1, 2.5, and 5 mM PZA from 72 h postfertilization (hpf). Different endpoints such as mortality, morphology changes in the size and shape of the liver, histological changes, transaminase analysis and apoptosis, markers of oxidative and genetic damage, as well as the expression of certain genes were selected to evaluate PZA-induced hepatotoxicity. Our results confirm the manner of PZA dose-dependent hepatotoxicity. PZA was found to induce marked injury in zebrafish larvae, such as liver atrophy, elevations of transaminase levels, oxidative stress, and hepatocyte apoptosis. To further understand the mechanism behind PZA-induced hepatotoxicity, changes in gene expression levels in zebrafish larvae exposed to PZA for 72 h postexposure (hpe) were determined. The results of this study demonstrated that PZA decreased the expression levels of liver fatty acid binding protein (L-FABP) and its target gene, peroxisome proliferator-activated receptor ␣ (PPAR-␣), and provoked more severe oxidative stress and hepatitis via the upregulation of inflammatory cytokines such as tumor necrosis factor alpha (TNF-␣) and transforming growth factor ␤ (TGF-␤). These findings suggest that L-FABP-mediated PPAR-␣ downregulation appears to be a hepatotoxic response resulting from zebrafish larva liver cell apoptosis, and L-FABP can be used as a biomarker for the early detection of PZA-induced liver damage in zebrafish larvae. P yrazinamide (PZA) is an important first-line drug in tuberculosis (TB) combination chemotherapy and is used during the initial 2 months of treatment for its remarkable sterilizing activity (1). Hepatotoxicity is the major adverse effect of PZA and usually occurs in the first 2 months of treatment (2). Previously reported studies showed a high incidence of hepatotoxicity with a high dosage of 40 to 70 mg/kg of body weight and a low rate of liver injury with a daily dose of Ͻ35 mg/kg (3). Although a reduction of the clinical dose considerably decreased the rate of PZA-induced hepatotoxic side effects, PZA is still considered to induce higher hepatotoxicity than other first-line antituberculosis drugs (4, 5). PZA hepatotoxicity cannot be ignored; however, little is known about the exact mechanism of PZA-induced hepatotoxicity.Previous research, by using microarray analyses and proteomics studies, found that metabolism, inflammation, and oxidative stress pathways were probably involved in PZA-induced hepatotoxicity (6, 7). A recent investigation showed that the metabolite 5-hydroxypyrazinoic acid (5-OH-PA) is responsible for PZAinduced hepatotoxicity (8). Despite an increasing number of researchers who are trying to reevaluate the hepatotoxic potentia...

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“…Several studies have described the applicability of the L-FABP protein to the detection of hepatic injury in diseases such as hepatocellular adenoma 12 and chronic HCV infection 13 .…”

Section: Groupsmentioning

confidence: 99%

L-FABP and I-FABP expression in newborn rats changes inversely in the model of necrotizing enterocolitis

et al. 2014

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Brazil. Mentor, conception and design of the study, manuscript writing and critical revision. ABSTRACT PURPOSE:To determine the expression of hepatic L-FABP and intestinal I-FABP in an experimental model of necrotizing enterocolitis (NEC) in neonatal rats. METHODS:Newborn Sprague-Dawley rats were divided into four groups: Control (C1) -exclusive breastfeeding at the first and sixth procedures (C6), NEC1 -fed formula milk and submitted to hypoxia and hypothermia at the first and sixth procedures (NEC6). The newborn pups were fed twice a day for three days, for a total of six procedures. Samples were collected for morphometric evaluation (body weight, liver weight, liver weight/body weight ratio, intestinal weight and intestinal/body weight ratio) and for immunohistochemical and Western blotting analysis. The values obtained were analyzed statistically, with the level of significance set at p<0.05. RESULTS:Morphometric measurements showed reduction of body and liver weights in the NEC group (p<0.05). Both immunohistochemistry and western blotting revealed that L-FABP expression in the liver was decreased and I-FABP expression in the ileum was increased in the NEC group (p<0.05).CONCLUSION: L-FABP and I-FABP expression changed inversely in the rat NEC model. These findings can contribute to a better diagnosis of NEC in human newborns.

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Liver Fatty Acid-binding Protein Is A Diagnostic Marker to Detect Liver Injury Due to Chronic Hepatitis C Infection

Cited by 35 publications

References 31 publications

Liver fatty acid-binding protein as a diagnostic marker for non-alcoholic fatty liver disease

Liver fatty acid-binding protein as a diagnostic marker for non-alcoholic fatty liver disease

Liver Fatty Acid Binding Protein Deficiency Provokes Oxidative Stress, Inflammation, and Apoptosis-Mediated Hepatotoxicity Induced by Pyrazinamide in Zebrafish Larvae

L-FABP and I-FABP expression in newborn rats changes inversely in the model of necrotizing enterocolitis

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