Association of tumor necrosis factor‐α gene promoter polymorphism at sites ‐308 and ‐238 with non‐alcoholic fatty liver disease: A meta‐analysis

Ji-kai, Wang; Feng, Zhewei; Li, Yingchun; Li, Qingyan; Tao, Xingyong

doi:10.1111/j.1440-1746.2011.06978.x

Cited by 51 publications

(35 citation statements)

References 30 publications

(62 reference statements)

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“…TNF-α polymorphisms have been shown to be strongly associated with the risk of developing NAFLD especially in Chinese population and this was confirmed in a meta-analysis by Wang et al [11].…”

Section: Introductionmentioning

confidence: 68%

PNPLA3 and TNF-<i>α</i> G238A Genetic Polymorphisms in Egyptian Patients with Different Grades of Severity of NAFLD

Hegazy¹,

Samie²,

Ezzat³

et al. 2016

OJGas

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Introduction: There is growing evidence that genetic and environmental factors play an important role in the development and progression of non-alcoholic fatty liver disease (NAFLD). We investigated the association of single nucleotide polymorphism (SNP) rs738409 in PNPLA3 gene and TNF-α G238A polymorphism with the development and severity of NAFLD in an overweight and obese Egyptian population. Material and Methods: 100 overweight and obese patients with NAFLD and 30 control subjects were enrolled. All NAFLD patients underwent a confirmatory biopsy. Laboratory investigations included fasting plasma glucose, kidney and liver function tests, liver enzymes, lipid profile and hepatitis markers. Abdominal ultrasound was performed and all subjects were genotyped for (rs738409) PNPLA3 and (rs361525) TNF-α gene polymorphisms using polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Results: The homozygous GG genotype of the PNPLA3 was most frequent among patients with NASH (26%) as compared to borderline NASH (20.5%) and simple steatosis (20%). Higher serum levels of transaminases were observed in NAFLD patients and controls who were carriers of the G allele of rs738409, but this was not statistically significant. Regarding the TNF-α G238A SNP; the frequency of the A allele was significantly higher in NAFLD patients (20%) compared to controls (5%) (p value = 0.006). The highest TNF G allele frequency was observed in the NASH group (88%) and this was statistically significant (p value = 0.009). Conclusion: Our study confirmed the association of the PNPLA3 (rs738409) and TNF-α promoter region G238A polymorphisms with susceptibility to NAFLD and its progression. M. A. Hegazy et al.54

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Section: Introductionmentioning

confidence: 68%

PNPLA3 and TNF-<i>α</i> G238A Genetic Polymorphisms in Egyptian Patients with Different Grades of Severity of NAFLD

Hegazy¹,

Samie²,

Ezzat³

et al. 2016

OJGas

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“…Furthermore, a recent meta-analysis has demonstrated that polymophisms of TNF-α (-238) is particularly associated with the susceptibility to NAFLD [142] . TNF-α has also been previously known to be an important cytokine that regulates insulin resistance by affecting insulin receptor substrate-1 (IRS-1) and insulin receptor kinase (IRK) in the insulin signal transduction pathway [142] . Nevertheless, the involvement of TNF-α in insulin resistance is debatable.…”

Section: Genes That Affect Cytokines Productionmentioning

confidence: 99%

“…Wang et al [142] 2012 Polymophisms of TNF-α are associated with the susceptibility to NAFLD Insulin resistance and hepatic inflammation are related Insulin signal transduction pathway does contribute to the progression of NAFLD…”

Section: Tnf-αmentioning

confidence: 99%

Proteomic and genomic studies of non-alcoholic fatty liver disease - clues in the pathogenesis

Lim

Dillon

Miller

2014

WJG

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Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder that covers wide spectrum of liver pathology. NAFLD is strongly associated with liver inflammation, metabolic hyperlipidaemia and insulin resistance. Frequently, NAFLD has been considered as the hepatic manifestation of metabolic syndrome. The pathophysiology of NAFLD has not been fully elucidated. Some patients can remain in the stage of simple steatosis, which generally is a benign condition; whereas others can develop liver inflammation and progress into non-alcoholic steatohepatitis, fibrosis, cirrhosis and hepatocellular carcinoma. The mechanism behind the progression is still not fully understood. Much ongoing proteomic researches have focused on discovering the unbiased circulating biochemical markers to allow early detection and treatment of NAFLD. Comprehensive genomic studies have also begun to provide new insights into the gene polymorphism to understand patientdisease variations. Therefore, NAFLD is considered a complex and mutifactorial disease phenotype resulting from environmental exposures acting on a susceptible polygenic background. This paper reviewed the current status of proteomic and genomic studies that have contributed to the understanding of NAFLD pathogenesis. For proteomics section, this review highlighted functional proteins that involved in: (1) transportation; (2) metabolic pathway; (3) acute phase reaction; (4) antiinflammatory; (5) extracellular matrix; and (6) immune system. In the genomic studies, this review will discuss genes which involved in: (1) lipolysis; (2) adipokines; and (3) cytokines production. Key words: Non-alcoholic fatty liver disease; Proteomics; Genomics; Metabolic syndrome; Pathophysiology Core tip: Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder in Western populations. NAFLD can occur as a spectrum diseases, from simple steatosis, to non-alcoholic steatohepatitis characterised by hepatocellular injury and inflammation, to cirrhosis and hepatocellular carcinoma. This paper reviewed the current status of proteomic and genomic studies that have contributed to the understanding of NAFLD pathogenesis. This review highlighted several functional proteins and genetic polymoprhisms; particular those involved in insulin resistance, triglycerides metabolism and hepatic inflammation. It is hoped that this review will offer further insights into the pathophysiology of NAFLD.

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“…However, frequencies of variants -1031C and -863A were more prevalent in subjects with NASH in a different study (75). A meta-analysis evaluating polymorphisms in TNF-α confirmed the relationship of the -238 polymorphism with NAFLD, whereas the -308 polymorphism was not determined as a susceptible factor (76). Additionally, TNF-α G-308A, G-238A and C-863A polymorphisms are also related to HCC in Asians populations (77).…”

Section: Gene Polymorphisms In Mediators Of Related Cytokinesmentioning

confidence: 83%

Development of gene polymorphisms in meditators of nonalcoholic fatty liver disease

Wang

Gong

2017

Biomedical Reports

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Abstract. Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease worldwide, the morbidity of which closely correlates with diversity of ethnicity, minority, family and location. Its histology spans from simple steatosis, to nonalcoholic steatohepatitis, which ultimately results in fibrosis, cirrhosis and hepatocellular carcinoma. The accelerating prevalence of NAFLD is due to an incremental incidence of metabolic syndrome that is distinguished by dyslipidemia, glucose impairment, obesity, excessive oxidative stress and adipocytokine impairment. Additionally, the pathogenesis of NAFLD is thought to be a multifactorial and complicated disease associated with lifestyle habits, nutritional factors and genetics. However, the pathogenesis and underlying mechanism in the development of NAFLD caused by genetics remains unclear. People have been increasingly emphasizing on the relationship between NAFLD and gene polymorphisms in recent years, with the aim of having a comprehensive elucidation of associated gene polymorphisms influencing the pathogenesis of the disease. In the current article, the authors attempted to critically summarize the most recently identified gene polymorphisms from the facets of glucose metabolism, fatty acid metabolism, oxidative stress and related cytokines in NAFLD that contribute to promoting the progression of the disease.

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Association of tumor necrosis factor‐α gene promoter polymorphism at sites ‐308 and ‐238 with non‐alcoholic fatty liver disease: A meta‐analysis

Abstract: This meta-analysis suggested that TNF-α gene promoter polymorphism at position -238 but not -308 might be a risk factor for NAFLD.

Cited by 51 publications

References 30 publications

PNPLA3 and TNF-<i>α</i> G238A Genetic Polymorphisms in Egyptian Patients with Different Grades of Severity of NAFLD

PNPLA3 and TNF-<i>α</i> G238A Genetic Polymorphisms in Egyptian Patients with Different Grades of Severity of NAFLD

Proteomic and genomic studies of non-alcoholic fatty liver disease - clues in the pathogenesis

Development of gene polymorphisms in meditators of nonalcoholic fatty liver disease

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Association of tumor necrosis factor‐α gene promoter polymorphism at sites ‐308 and ‐238 with non‐alcoholic fatty liver disease: A meta‐analysis

Abstract: This meta-analysis suggested that TNF-α gene promoter polymorphism at position -238 but not -308 might be a risk factor for NAFLD.

Cited by 51 publications

References 30 publications

PNPLA3 and TNF-&lt;i&gt;α&lt;/i&gt; G238A Genetic Polymorphisms in Egyptian Patients with Different Grades of Severity of NAFLD

PNPLA3 and TNF-&lt;i&gt;α&lt;/i&gt; G238A Genetic Polymorphisms in Egyptian Patients with Different Grades of Severity of NAFLD

Proteomic and genomic studies of non-alcoholic fatty liver disease - clues in the pathogenesis

Development of gene polymorphisms in meditators of nonalcoholic fatty liver disease

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Product

Resources

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PNPLA3 and TNF-<i>α</i> G238A Genetic Polymorphisms in Egyptian Patients with Different Grades of Severity of NAFLD

PNPLA3 and TNF-<i>α</i> G238A Genetic Polymorphisms in Egyptian Patients with Different Grades of Severity of NAFLD