Polymorphisms of the tumour necrosis factor‐α gene, coronary heart disease and obesity

Herrmann, Stefan; Ricard, Sylvain; Nicaud, Viviane; Mallet, Christine; Arveiler, Dominique; Evans, Alun; Ruidavets, Jean‐Bernard; Luc, Gérald; Bara, L.; Parra, Henri‐Joseph; Poirier, Odette; Cambien, François

doi:10.1046/j.1365-2362.1998.00244.x

Cited by 212 publications

(123 citation statements)

References 49 publications

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“…Our data confirm some previous studies that investigated Caucasian populations and failed to demonstrate that this locus could be a marker for greater risk of CAD. The same studies affirm that the allelic distribution is different according to the geographical origin of the study group (ranging from 24% to 12% for the rare allele) (25,30). However, in contrast to other published data (26,31), this may be due to different genetic and environmental risk factors or to different selection criteria of CAD patients.…”

Section: Discussionmentioning

confidence: 62%

“…Previous cardiovascular studies have investigated the association between several SNPs located in the promoter region of the TNF-a gene and CAD or atherosclerosis (24)(25)(26)(27), but conclusive data regarding the role of TNF-a genotypes in CAD pathogenesis is need-ed. The present study investigated the association between two biallelic polymorphisms of the TNF-a gene and their relation to CAD in an Arab African population.…”

Section: Discussionmentioning

confidence: 99%

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–308G>A and –1031T>C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery disease

Ghazouani

Khalifa²,

Abboud³

et al. 2009

Clinical Chemistry and Laboratory Medicine

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

–308G>A and –1031T>C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery disease

Ghazouani

Khalifa²,

Abboud³

et al. 2009

Clinical Chemistry and Laboratory Medicine

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“…Our findings suggest that the A allele of the -238 polymorphism may be responsive to dietary fatty acid intake, as has been shown for the -308 A allele. 1,3,27,28,37 However, understanding the inflammatory impact of this polymorphism needs to be confirmed. Measures of circulating TNFA or TNFA receptor levels may be informative in this respect.…”

Section: Discussionmentioning

confidence: 99%

The tumor necrosis factor-α gene -238 G>A polymorphism, dietary fat intake, obesity risk and serum lipid concentrations in black and white South African women

et al. 2012

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BACKGROUND/OBJECTIVES: This study explored interactions between dietary fat intake and the tumor necrosis factor-a gene (TNFA) -238 G4A polymorphism (rs361525) on adiposity and serum lipid concentrations in apparently healthy premenopausal black and white South African (SA) women. SUBJECTS/METHODS: Normal-weight (N ¼ 107) and obese (N ¼ 120) black, and normal-weight (N ¼ 89) and obese (N ¼ 62) white SA women underwent measurements of body composition, fasting lipids and dietary intake, and were genotyped for the -238 G4A polymorphism. RESULTS: Black women had a higher -238 GA genotype frequency than white women (Po0.001), but there were no differences between body mass index groups. Black women with the -238 A allele had a greater body fat % than those with the GG genotype (Po0.001). Further, in black women, with increasing polyunsaturated:saturated fat ratio and omega-6 (n-6):omega-3 (n-3) ratio, high-density lipoprotein-cholesterol (HDL-C) concentrations decreased, and total cholesterol (T-C):HDL-C ratio increased in those with the GA genotype but not the GG genotype. In addition, with increasing n-3 polyunsaturated fatty acid intake (percentage of total energy intake, %E), T-C:HDL-C ratio decreased in those with the GA genotype, but not in those with the GG genotype. In white SA women, with increasing eicosapentaenoic acid (%E) intake, low-density lipoprotein-cholesterol concentrations decreased in those with the GG genotype but not the GA genotype. CONCLUSIONS: The -238 G4A polymorphism was associated with body fatness in black women. Interactions between -238 G4A genotypes and dietary fat intake on serum lipids and adiposity differed depending on dietary fat intake, but those for serum lipids were not the same in black and white SA women.

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“…5 TNF-a binds to two receptors on the cell surface: p75 and p55. Our previous result prompted us to screen the p55 receptor gene (TNF receptor superfamily, member 1A -TNFRSF1A) for polymorphisms, because it has been shown that endothelial cell responses to TNF-a, such as expression of tissue factor and adhesion molecules by mononuclear cells (which may be important in the pathogenesis of atherosclerosis) are mediated predominantly by this receptor.…”

Section: Introductionmentioning

confidence: 99%

Polymorphism R92Q of the tumour necrosis factor receptor 1 gene is associated with myocardial infarction and carotid intima-media thickness – The ECTIM, AXA, EVA and GENIC Studies

et al. 2003

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The TNFRSF1A gene was screened for polymorphisms in 95 subjects with premature myocardial infarction (MI), who also had one parent who had an MI. A total of 10 polymorphisms were found: three in the promoter region, two in exons and five in introns. All polymorphisms were genotyped in ECTIM, a case-control study of MI (1815 subjects). The nonsynonymous 92Q allele was found in 1.8, 1.0 and 1.7% of controls from Strasbourg, Belfast and Glasgow -respectively; in cases: 4.2, 2.2 and 3.2%. The populationadjusted odds ratio (OR) for MI associated with allele Q carrying was 2.15 (95% CI: 1.09 -4.23). To check its possible implication in atherosclerosis, this polymorphism was then genotyped in the AXA Study (ultrasound examinations of carotid and femoral arteries in the context of an employment medical examination, 733 subjects), the EVA Study (ultrasound examinations of carotid arteries in a study of cognitive and vascular ageing, 1092 subjects) and the GENIC Study (on brain infarction (BI), 912 subjects). In the AXA Study, among smokers, carrying the 92Q allele was positively associated with the presence of a carotid plaque (OR 5.07; 95% CI: 1.64 -15.63) and with a thickening of the carotid intima-media thickness (IMT) (0.59 (0.11) vs 0.54 (0.11), P ¼ 0.045). In the EVA Study, carriers of allele 92Q had an increased mean carotid IMT (0.70 (0.09) vs 0.67 (0.13), P ¼ 0.02). No significant association of the 92Q allele was found with BI in the GENIC Study. Overall, these results may suggest that carriers of the 92Q allele may be at increased risk of atherosclerosis.

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Polymorphisms of the tumour necrosis factor‐α gene, coronary heart disease and obesity

Abstract: These results suggest that polymorphisms of the TNF-alpha gene are unlikely to contribute to CHD risk in an important way, but the TNF-alpha/-308 polymorphism should be investigated further in relation to obesity.

Cited by 212 publications

References 49 publications

–308G>A and –1031T>C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery disease

–308G>A and –1031T>C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery disease

The tumor necrosis factor-α gene -238 G>A polymorphism, dietary fat intake, obesity risk and serum lipid concentrations in black and white South African women

Polymorphism R92Q of the tumour necrosis factor receptor 1 gene is associated with myocardial infarction and carotid intima-media thickness – The ECTIM, AXA, EVA and GENIC Studies

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