The Effect of Taurine on Hepatic Steatosis Induced by Thioacetamide in Zebrafish (Danio rerio)

Hammes, Thaís Ortiz; Pedroso, Fiona L.; Hartmann, Carolina Rigatti; Escobar, Thayssa Dalla Costa; Fracasso, Laisa Beduschi; Rosa, Darlan Pase da; Marroni, Norma Possa; Porawski, Marilene; Silveira, Themis Reverbel da

doi:10.1007/s10620-011-1931-4

Cited by 27 publications

(18 citation statements)

References 51 publications

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“…Continuous treatment with TAA for 12 weeks leads to development of hepatic fibrosis and induction of HCC (153). TAA-induced steatosis has been successfully treated by administration of taurine, which functions at least in part, by decreasing oxidative stress (65). …”

Section: Modeling Human Liver Disease Mechanisms In Zebrafishmentioning

confidence: 99%

Zebrafish Models of Human Liver Development and Disease

Wilkins

Pack

2013

Comprehensive Physiology

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The liver performs a large number of essential synthetic and regulatory functions that are acquired during fetal development and persist throughout life. Their disruption underlies a diverse group of heritable and acquired diseases that affect both pediatric and adult patients. Although experimental analyses used to study liver development and disease are typically performed in cell culture models or rodents, the zebrafish is increasingly used to complement discoveries made in these systems. Forward and reverse genetic analyses over the past two decades have shown that the molecular program for liver development is largely conserved between zebrafish and mammals, and that the zebrafish can be used to model heritable human liver disorders. Recent work has demonstrated that zebrafish can also be used to study the mechanistic basis of acquired liver diseases. Here, we provide a comprehensive summary of how the zebrafish has contributed to our understanding of human liver development and disease.

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Section: Modeling Human Liver Disease Mechanisms In Zebrafishmentioning

confidence: 99%

Zebrafish Models of Human Liver Development and Disease

Wilkins

Pack

2013

Comprehensive Physiology

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“…The increased level of serum ammonia in OHE mice was ascribed to the impairment of urea cycle, which normally removes ammonia from body. TAU supplement could ameliorate both liver dysfunction and encephalopathy disorder as revealed by decreased contents of serum ammonia, ALT and AST, and increased level of SOD (Dorgru-Abbasoglu et al 2001;Hammes et al 2012). Compared with CTRL mice, mice in OHE group showed poor ability of reflexes and task performance with significantly elevated NSS of OHE group at 72 h after TAA administration, revealing severely impaired brain function due to TAA intoxication.…”

Section: Discussionmentioning

confidence: 93%

“…(Color figure online) could ameliorate liver injury induced by TAA via its free radical scavenging activity Hammes et al 2012) and enhanced intracellular production of glutathione (GSH) (Das et al 2010). Overwhelmed by the TAA-induced oxidative stress, hepatic TAU and GSH were largely consumed and significantly decreased in OHE group as a self-defense mechanism.…”

Section: Discussionmentioning

confidence: 99%

A pilot study of the onset of hepatic encephalopathy (OHE) in mice induced by thioacetamide and the protective effect of taurine by holistic metabolic characterization

Wei

Wang

et al. 2014

Metabolomics

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Hepatic encephalopathy (HE) is a severe neuropsychiatric complication due to acute or chronic liver failure. In this work, an acute thioacetamide induced HE mice model was established to investigate the metabolic events in the onset of HE (OHE) and the protective role of taurine (TAU). Sera for biochemical evaluation, and livers and cortexes for histopathological inspection and NMRbased metabolomic investigation were collected. Principal component analysis and orthogonal partial least squaresdiscriminant analysis were performed to excavate differential metabolites of OHE, and explore the protective role of TAU. Metabolites pathway analysis was performed on significant metabolites selected based on loading/S-plots and fold change plots to identify biologically meaningful metabolic patterns and relevant pathways. The most affected pathways in OHE mice were those along the liverbrain axis: among them, the alanine, aspartate and glutamate metabolism was the most important. TAU showed better performance in improving the disturbed metabolism in the cortex than in the liver of OHE mice. This pilot study based on metabolomics approach and pathway analysis should help to understand HE systematically, and to develop new therapy for HE.

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“…Zebrafish are indeed able to respond to LPS, however with much lower sensitivity than mammals and via a tlr4/myd88 -independent signaling pathway[24,28]. Among the few studies that evaluated tnf-a expression in the liver of zebrafish, Sapp observed an elevation of tnf-a in fructose-treated larvae and Hammes in thiocetamide-treated fish[20,29]. Although there was no direct evidence in our study, these cited findings conducted us to the following conclusions: tnf-a is not promptly induced by LPS in zebrafish exposed to ethanol as occurring in mammals and its activation mechanism seems to be associated to more aggressive hepatotoxicants.…”

Section: Discussionmentioning

confidence: 99%

“…To date, very few data are available regarding the effect of chronic ethanol exposure on hepatic adipor2 . Hammes et al[29] observed decreased mRNA expression of hepatic adipor2 and sirt-1 and increased tnf-a in a model of NAFLD induced by thioacetamide in zebrafish. Possibly, thioacetamide, a more aggressive liver toxicant, contributed to down regulate adipor2 .…”

Section: Discussionmentioning

confidence: 99%

Chronic exposure to ethanol causes steatosis and inflammation in zebrafish liver

Schneider¹,

Gregório²,

Cruz³

et al. 2017

WJH

Self Cite

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AIMTo evaluate the effects of chronic exposure to ethanol in the liver and the expression of inflammatory genes in zebrafish.METHODSZebrafish (n = 104), wild type, adult, male and female, were divided into two groups: Control and ethanol (0.05 v/v). The ethanol was directly added into water; tanks water were changed every two days and the ethanol replaced. The animals were fed twice a day with fish food until satiety. After two and four weeks of trial, livers were dissected, histological analysis (hematoxilin-eosin and Oil Red staining) and gene expression assessment of adiponectin, adiponectin receptor 2 (adipor2), sirtuin-1 (sirt-1), tumor necrosis factor-alpha (tnf-a), interleukin-1b (il-1b) and interleukin-10 (il-10) were performed. Ultrastructural evaluations were conducted at fourth week.RESULTSExposing zebrafish to 0.5% ethanol developed intense liver steatosis after four weeks, as demonstrated by oil red staining. In ethanol-treated animals, the main ultrastructural changes were related to cytoplasmic lipid particles and droplets, increased number of rough endoplasmic reticulum cisterns and glycogen particles. Between two and four weeks, hepatic mRNA expression of il-1b, sirt-1 and adipor2 were upregulated, indicating that ethanol triggered signaling molecules which are key elements in both hepatic inflammatory and protective responses. Adiponectin was not detected in the liver of animals exposed and not exposed to ethanol, and il-10 did not show significant difference.CONCLUSIONData suggest that inflammatory signaling and ultrastructural alterations play a significant role during hepatic steatosis in zebrafish chronically exposed to ethanol.

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The Effect of Taurine on Hepatic Steatosis Induced by Thioacetamide in Zebrafish (Danio rerio)

Abstract: Taurine seems to improve hepatic steatosis by reducing oxidative stress and increasing SIRT1 expression.

Cited by 27 publications

References 51 publications

Zebrafish Models of Human Liver Development and Disease

Zebrafish Models of Human Liver Development and Disease

A pilot study of the onset of hepatic encephalopathy (OHE) in mice induced by thioacetamide and the protective effect of taurine by holistic metabolic characterization

Chronic exposure to ethanol causes steatosis and inflammation in zebrafish liver

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