Polymorphisms of microsomal triglyceride transfer protein gene and manganese superoxide dismutase gene in non-alcoholic steatohepatitis

Namikawa, Chikako; Zhang, Shuping; Vyselaar, John Raynor; Nozaki, Yasuko; Nemoto, Yuiko; Ono, Masafumi; Akisawa, Naoaki; Saibara, Toshiji; Hiroi, Makoto; Enzan, Hideaki; Onishi, Saburo

doi:10.1016/j.jhep.2004.01.028

Cited by 219 publications

(178 citation statements)

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“…With this said, however, studies performed in the UK with a larger cohort of alcoholic patients showed no association among the valine-alanine SOD2 polymorphism, alcohol-dependent markers of oxidative stress, and liver fibrosis [132]. Preliminary studies indicate that the SOD2 polymorphism may be correlated to fibrosis in NAFLD patients [133].…”

Section: Genetic Factors Determining the Pathobiology Of Fatty Livermentioning

confidence: 93%

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

Mantena

King

Andringa

et al. 2008

Free Radical Biology and Medicine

372

297

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Fatty liver disease associated with chronic alcohol consumption or obesity/type 2 diabetes has emerged as a serious public health problem. Steatosis, accumulation of triglyceride in hepatocytes, is now recognized as a critical "first-hit" in the pathogenesis of liver disease. It is proposed that steatosis "primes" the liver to progress to more severe liver pathologies when individuals are exposed to subsequent metabolic and/or environmental stressors or "second-hits". Genetic risk factors can also influence the susceptibility and severity of fatty liver disease. Furthermore, oxidative stress, disrupted nitric oxide (NO) signaling, and mitochondrial dysfunctional are proposed to be key molecular events that accelerate or worsen steatosis and initiate progression to steatohepatitis and fibrosis. This review article will discuss the following topics regarding the pathobiology and molecular mechanisms responsible for fatty liver disease: 1) the "two-hit" or "multi-hit" hypothesis; 2) the role of mitochondrial bioenergetic defects and oxidant stress; 3) interplay between NO and mitochondria in fatty liver disease; 4) genetic risk factors and oxidative stress responsive genes; and 5) the feasibility of antioxidants for treatment.

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Section: Genetic Factors Determining the Pathobiology Of Fatty Livermentioning

confidence: 93%

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

Mantena

King

Andringa

et al. 2008

Free Radical Biology and Medicine

372

297

View full text Add to dashboard Cite

show abstract

“…18,[21][22][23] In NAFLD, lipid accumulation within the liver (steatosis) may result from several mechanisms: increased fat synthesis, increased fat delivery, decreased fat export and/or decreased fat oxidation. [23][24][25][26][27][28] IR plays an important role in NAFLD development and evolution, and NAFLD also contributes towards worsening of IR.…”

Section: Pathophysiologymentioning

confidence: 99%

Nonalcoholic fatty liver disease and bariatric surgery: a comprehensive review

2017

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CONTEXT AND OBJECTIVE: Nonalcoholic fatty liver disease (NAFLD) has been increasingly diagnosed worldwide and is now recognized as a source of public health concern. It comprises a wide spectrum of histological features that range from simple steatosis to severe forms of fibrosis, steatohepatitis and even cirrhosis. The impact of bariatric surgery on the course of NAFLD in individuals with obesity has been extensively studied. DESIGN AND SETTING: Narrative review; public university hospital. METHODS: A comprehensive review was conducted based on an online search on the electronic databases MEDLINE and LILACS using the MeSH terms "fatty liver" and "bariatric surgery". RESULTS:The exact mechanisms that lead to improvement in NAFLD following bariatric surgery are not completely understood. Since Roux-en-Y gastric bypass (RYGB) is the bariatric surgical procedure most performed worldwide, it is also the one from which the effects on NAFLD have been most studied, although there is also consistent evidence regarding the effects from gastric banding, sleeve gastrectomy and biliopancreatic diversions. CONCLUSION: According to the currently available evidence, bariatric surgery leads to significant improvement in NAFLD. Further research, especially by means of randomized controlled trials enrolling larger cohorts of individuals, is needed to determine the optimal procedure for this group of subjects. RESUMO CONTEXTO E OBJETIVO:A doença hepática gordurosa não alcoólica (DHGNA) tem sido diagnosticada com maior frequência em todo o mundo na atualidade, sendo agora reconhecida como motivo de preocupação em saúde pública. Abrange um amplo espectro de alterações histológicas que variam desde a simples esteatose até formas graves de fibrose, esteato-hepatite e até cirrose. O impacto da cirurgia bariátrica sobre o curso da DHGNA em indivíduos com obesidade tem sido profundamente estudado. TIPO DE ESTUDO E LOCAL: Revisão narrativa; hospital universitário público. MÉTODOS: Uma revisão abrangente da literatura foi conduzida baseada na pesquisa on-line nas bases de dados eletrônicas MEDLINE e LILACS por meio dos termos MeSH "fígado gorduroso" e "cirurgia bariátrica". RESULTADOS: Os mecanismos exatos que levam à melhora da DHGNA após a cirurgia bariátrica não são completamente conhecidos. Como o bypass gástrico em Y de Roux é a cirurgia bariátrica mais realizada em todo o mundo, é também o procedimento cujos efeitos sobre DHGNA foram mais estudados, embora haja também evidências consistentes sobre os efeitos de banda gástrica, gastrectomia vertical e derivações biliopancreáticas. CONCLUSÃO: De acordo com as evidências atualmente disponíveis, a cirurgia bariátrica leva à melhora significativa da DHGNA. Mais estudos, especialmente por meio de ensaios clínicos randomizados e controlados, recrutando coortes maiores de indivíduos, são necessários para determinar o melhor procedimento para esse grupo de pacientes.

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“…9 MTP polymorphisms that decrease expression increase the risk of NAFLD. 10 Nuclear receptors that regulate lipid metabolism in the liver are potential contributors to fatty liver. Thus, increased activity of peroxisome proliferator-activated receptors (PPAR␥) has been directly associated with fatty liver formation.…”

mentioning

confidence: 99%

Molecular characterization of the role of orphan receptor small heterodimer partner in development of fatty liver

et al. 2007

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The orphan receptor Small Heterodimer Partner (SHP, NROB2) regulates metabolic pathways, including hepatic bile acid, lipid, and glucose homeostasis. We reported that SHP-deletion in leptin-deficient OB ؊/؊ mice increases insulin sensitivity, and prevents the development of fatty liver. The prevention of steatosis in OB ؊/؊ /SHP ؊/؊ double mutants is not due to decreased body weight but is associated with increased hepatic very-low-density lipoprotein (

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Polymorphisms of microsomal triglyceride transfer protein gene and manganese superoxide dismutase gene in non-alcoholic steatohepatitis

Cited by 219 publications

References 33 publications

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

Nonalcoholic fatty liver disease and bariatric surgery: a comprehensive review

Molecular characterization of the role of orphan receptor small heterodimer partner in development of fatty liver

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