Influence of TNF gene polymorphisms in Japanese patients with NASH and simple steatosis

Tokushige, Katsutoshi; Takakura, Mihoko; Tsuchiya-Matsushita, Noriko; Taniai, Makiko; Hashimoto, Etsuko; Shiratori, Keiko

doi:10.1016/j.jhep.2007.01.028

Cited by 141 publications

(107 citation statements)

References 39 publications

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“…Familial clustering and ethnic differences in susceptibility indicate that genetic factors may be important risk determinants for development and progression of NAFLD/ NASH [32][33][34][35][36]. Variation in the enzyme adiponutrin (patatin-like phospholipase domain-containing protein 3; PNPLA3) is a major genetic determinant of hepatic steatosis and fibrosis [33][34][35].…”

Section: Clinical Featuresmentioning

confidence: 99%

Evidence-based clinical practice guidelines for nonalcoholic fatty liver disease/nonalcoholic steatohepatitis

et al. 2015

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Nonalcoholic fatty liver disease (NAFLD) is currently the most common cause of chronic liver disease in industrialized countries worldwide, and has become a serious public health issue not only in Western countries but also in many Asian countries including Japan. Within the wide spectrum of NAFLD, nonalcoholic steatohepatitis (NASH) is a progressive form of disease, which often develops into liver cirrhosis and increases the risk of hepatocellular carcinoma. In turn, a large proportion of NAFLD/NASH is the liver manifestation of metabolic syndrome, suggesting that NAFLD/NASH plays a key role in the pathogenesis of systemic atherosclerotic diseases. Currently, a definite diagnosis of NASH requires liver biopsy, though various noninvasive measures are under development. The mainstays of prevention and treatment of NAFLD/NASH include dietary restriction and exercise; however, pharmacological approaches are often necessary.Currently, vitamin E and thiazolidinedione derivatives are the most evidence-based therapeutic options, although the clinical evidence for long-term efficacy and safety is limited. This practice guideline for NAFLD/NASH, established by the Japanese Society of Gastroenterology in cooperation with The Japan Society of Hepatology, covers lines of clinical evidence reported internationally in the period starting from 1983 to January 2012, and each clinical question was evaluated using the GRADE system. Based on the primary release of the full version in Japanese, this English summary provides the core essentials of this clinical practice guideline comprising the definition, diagnosis, and current therapeutic recommendations for NAFLD/NASH in Japan.

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Section: Clinical Featuresmentioning

confidence: 99%

Evidence-based clinical practice guidelines for nonalcoholic fatty liver disease/nonalcoholic steatohepatitis

et al. 2015

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“…121 In addition, progression of NAFLD correlates with polymorphisms in the TNF-a promoter region and serum level of soluble Tumor Necrosis Factor (TNF)receptor-2. 122 It has been also shown that adipose tissue-derived IL-6 regulates hepatic IR via up-regulation of Suppressor of cytokine signaling 3 (SOCS3). 123 Indeed, over expression of SOCS-3 in the mouse liver causes IR and an increase in sterol regulatory element-binding protein (SREBP-1c) that regulates fatty acid synthesis.…”

Section: Cytokinesmentioning

confidence: 99%

The Riddle of Nonalcoholic Fatty Liver Disease: Progression From Nonalcoholic Fatty Liver to Nonalcoholic Steatohepatitis

Sharma

Mitnala

Vishnubhotla

et al. 2015

Journal of Clinical and Experimental Hepatology

127

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Nonalcoholic fatty liver (NAFL) is an emerging global epidemic which progresses to nonalcoholic steatohepatitis (NASH) and cirrhosis in a subset of subjects. Various reviews have focused on the etiology, epidemiology, pathogenesis and treatment of NAFLD. This review highlights specifically the triggers implicated in disease progression from NAFL to NASH. The integrating role of genes, dietary factors, innate immunity, cytokines and gut microbiome have been discussed. ( J CLIN EXP HEPATOL 2015;5:147-158)

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“…In a cohort including 66 Japanese patients with NASH, 36 with simple steatosis, and 100 control subjects, TNF␣ promoter polymorphisms were found to be more common in NASH than in simple steatosis. 137 …”

Section: Causes Of Liver Fat Accumulationmentioning

confidence: 99%

Fatty Liver

Kotronen

Yki‐Järvinen

2008

ATVB

702

264

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Abstract-Although the epidemic of obesity has been accompanied by an increase in the prevalence of the metabolic syndrome, not all obese develop the syndrome and even lean individuals can be insulin resistant. Both lean and obese insulin resistant individuals have an excess of fat in the liver which is not attributable to alcohol or other known causes of liver disease, a condition defined as nonalcoholic fatty liver disease (NAFLD) by gastroenterologists. The fatty liver is insulin resistant. Liver fat is highly significantly and linearly correlated with all components of the metabolic syndrome independent of obesity. Overproduction of glucose, VLDL, CRP, and coagulation factors by the fatty liver could contribute to the excess risk of cardiovascular disease associated with the metabolic syndrome and NAFLD. Both of the latter conditions also increase the risk of type 2 diabetes and advanced liver disease. The reason why some deposit fat in the liver whereas others do not is poorly understood.

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Influence of TNF gene polymorphisms in Japanese patients with NASH and simple steatosis

Cited by 141 publications

References 39 publications

Evidence-based clinical practice guidelines for nonalcoholic fatty liver disease/nonalcoholic steatohepatitis

Evidence-based clinical practice guidelines for nonalcoholic fatty liver disease/nonalcoholic steatohepatitis

The Riddle of Nonalcoholic Fatty Liver Disease: Progression From Nonalcoholic Fatty Liver to Nonalcoholic Steatohepatitis

Fatty Liver

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