Is Alanine Aminotransferase Level a Surrogate Biomarker of Hepatic Apoptosis in Nonalcoholic Fatty Liver Disease?

Canbakan, Billur; Şentürk, Hakan; Canbakan, Mustafa; Toptaş, Tayfur; Tabak, Ömür; Balcı, Huriye; Olgaç, Vakur; Özbay, Gülşen

doi:10.2217/bmm.09.88

Cited by 16 publications

(17 citation statements)

References 59 publications

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“…Apoptosis is the main process contributing to disease progression in NAFLD [22]. The significant association between steatosis and increased apoptosis suggests that hepatocyte lipid accumulation contributes to cell death [23].…”

Section: Discussionmentioning

confidence: 99%

“…The significant association between steatosis and increased apoptosis suggests that hepatocyte lipid accumulation contributes to cell death [23]. It is reported that caspase 3 activation was markedly increased in the liver of patients with severe steatohepatitis and in that of those with simple steatosis [22, 24]. Hepatocyte apoptosis may directly or indirectly promote inflammation [25].…”

Section: Discussionmentioning

confidence: 99%

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Melatonin in the Regulation of Liver Steatosis following Prenatal Glucocorticoid Exposure

Tiao

Huang

Chen

et al. 2014

BioMed Research International

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Nonalcoholic fatty liver disease patients are characterized by hepatic steatosis. Prenatal glucocorticoid overexposure can result in steatosis. In this study, we aimed to determine the mechanism and cellular apoptosis of prenatal glucocorticoid overexposure in rats and whether melatonin can rescue the prenatal glucocorticoid-induced steatosis and apoptosis in neonatal rats. Pregnant Sprague-Dawley rats at gestational days 14 to 21 were administered dexamethasone. Acute effects of prenatal programming liver were assessed at postnatal day 7. The expression of proteins involved in the apoptotic and methylation pathways was analyzed by RT-PCR and Western blotting. Apoptosis and steatosis were examined by histology staining. The liver steatosis and apoptosis were increased in prenatal glucocorticoid group more than in control group and decreased in melatonin group. The expression of leptin decreased in prenatal glucocorticoid and increased in melatonin group by liver RT-PCR and Western blot study. Caspase 3, TNF-α proteins expression, and TUNEL stains increased in prenatal glucocorticoid compared with control and decreased in melatonin group. The liver histone deacetylase, DNA methyltransferase activity, and DNA methylation were increased in prenatal glucocorticoid and decreased in melatonin group. The present study showed that the prenatal glucocorticoid induced programming liver steatosis at day 7 after delivery, possibly via altered leptin expression. Melatonin can reverse the methylation of leptin and decreased liver steatosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Melatonin in the Regulation of Liver Steatosis following Prenatal Glucocorticoid Exposure

Tiao

Huang

Chen

et al. 2014

BioMed Research International

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“…However, actually, in some chronic liver injury, there is no apparent change in ALT observed. Some studies have demonstrated that the serum ALT values do not correlate with the severity of the histopathological changes and the parameters of apoptosis in liver disease, and suggest histological assessment can more accurately determine the disease severity [38].…”

Section: Discussionmentioning

confidence: 99%

Early-Life Exposure to Bisphenol A Induces Liver Injury in Rats Involvement of Mitochondria-Mediated Apoptosis

Xia

Jiang

et al. 2014

PLoS ONE

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Exposure to bisphenol A (BPA), a monomer widely used to manufacture polycarbonate plastics, has been reported to be associated with abnormalities of liver function and hepatic damage. However, the molecular mechanism under the pathogenesis of hepatic injury is unclear. In this study, the effect of perinatal exposure to BPA at the reference dose of 50 µg/kg/day on the apoptotic index in the liver of rat offspring was investigated. Increased levels of ALT and enhanced cell apoptosis were observed in the liver of rat offspring at 15 and 21 weeks, and significantly increased activity of caspase-3 and caspase-9 and elevated levels of cytochrome c were also confirmed. In addition, significant change in the expression levels of Bcl-2 and Bax were found in BPA-treated offspring at 21 weeks. For in vitro experiments, liver mitochondria were isolated from neonatal rats and were treated with BPA. BPA treatment led to a significant increase in mitochondrial permeability transition. Moreover, the supernatant from BPA-treated mitochondria significantly increased apoptotic changes in nuclei isolated from liver tissue. In conclusion, the study demonstrates that BPA induces mitochondria-mediated apoptosis in hepatic cells, which may contribute to long-term hepatotoxicity induced by early-life exposure to BPA.

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“…In these latter studies, the diagnosis of steatosis was based on imaging methods or liver enzymes. Ultrasonography and ALT are less accurate than SteatoTest and FibroTest for the diagnosis of steatosis and fibrosis, respectively, which might explain conflicting results …”

Section: Discussionmentioning

confidence: 99%

Prognostic value of liver fibrosis and steatosis biomarkers in type-2 diabetes and dyslipidaemia

Perazzo

Munteanu

Ngo

et al. 2014

Aliment Pharmacol Ther

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Is Alanine Aminotransferase Level a Surrogate Biomarker of Hepatic Apoptosis in Nonalcoholic Fatty Liver Disease?

Abstract: Apoptosis and oxidative stress are the main processes contributing to disease progression in NAFLD. ALT values do not correlate with the parameters of apoptosis and oxidative stress. The disease severity can only be determined by liver biopsy.

Cited by 16 publications

References 59 publications

Melatonin in the Regulation of Liver Steatosis following Prenatal Glucocorticoid Exposure

Melatonin in the Regulation of Liver Steatosis following Prenatal Glucocorticoid Exposure

Early-Life Exposure to Bisphenol A Induces Liver Injury in Rats Involvement of Mitochondria-Mediated Apoptosis

Prognostic value of liver fibrosis and steatosis biomarkers in type-2 diabetes and dyslipidaemia

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