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      Association between TNF-α promoter G-308A and G-238A polymorphisms and obesity

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          Abstract

          Tumor necrosis factor-α (TNF-α), an adipokine, is produced in adipocytes, and the elevation of its levels has been linked to obesity and insulin resistance in some population. In this study the relationship between TNF-α promoter gene polymorphism and obesity in an Iranian population has been studied. Subjects were randomly selected from Tehran Cohort Lipid and Glucose Study. Adult participants placed in three groups according to their body mass index (BMI): BMI < 25, 25 ≤ BMI < 30, BMI ≥ 30 and under-18 subjects placed in two groups, under 85th percentile BMI and above 85th percentile. Finally, 244 persons were selected for G-308A and G-238A polymorphisms analysis. The FBS, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglyceride, cholesterol levels and blood pressure and HOMA of all subjects were measured. The polymorphism −308 and −238 were revealed by restriction fragment length polymorphism (RFLP; NCOI and MSPI) after the promoter site was amplified by PCR. The allele frequency of TNF-α polymorphism was in the Hardy–Weinberg equilibrium. There was no relation between BMI and the frequency of this allele. The fact that there is no association between G-308A and G-238A TNF-α promoter polymorphisms and obesity probably shows that it is not an important risk factor for obesity and consequently for cardiovascular disease.

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          Most cited references16

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          Effects of a polymorphism in the human tumor necrosis factor alpha promoter on transcriptional activation.

          Tumor necrosis factor alpha (TNF alpha) is a potent immunomodulator and proinflammatory cytokine that has been implicated in the pathogenesis of autoimmune and infectious diseases. For example, plasma levels of TNF alpha are positively correlated with severity and mortality in malaria and leishmaniasis. We have previously described a polymorphism at -308 in the TNF alpha promoter and shown that the rare allele, TNF2, lies on the extended haplotype HLA-A1-B8-DR3-DQ2, which is associated with autoimmunity and high TNF alpha production. Homozygosity for TNF2 carries a sevenfold increased risk of death from cerebral malaria. Here we demonstrate, with reporter genes under the control of the two allelic TNF promoters, that TNF2 is a much stronger transcriptional activator than the common allele (TNF1) in a human B cell line. Footprint analysis using DNase I and B cell nuclear extract showed the generation of a hypersensitive site at -308 and an adjacent area of protection. There was no difference in affinity of the DNA-binding protein(s) between the two alleles. These results show that this polymorphism has direct effects on TNF alpha gene regulation and may be responsible for the association of TNF2 with high TNF alpha phenotype and more severe disease in infections such as malaria and leishmaniasis.
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            Single base polymorphism in the human tumour necrosis factor alpha (TNF alpha) gene detectable by NcoI restriction of PCR product.

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              Human lymphotoxin and tumor necrosis factor genes: structure, homology and chromosomal localization.

              Human Tumor Necrosis Factor and Lymphotoxin are cytotoxic proteins which have similar biological activities and share 30 percent amino acid homology. The single copy genes which encode these proteins share several structural features: each gene is approximately three kilobase pairs in length and is interrupted by three introns. In addition, these genes are closely linked and have been mapped to human chromosome 6. However, only the last exons of both genes, which code for more than 80 percent of each secreted protein, are significantly homologous (56 percent).
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                Author and article information

                Contributors
                +98-21-22432500 , +98-21-22416264 , Hedayati@endocrine.ac.ir
                Journal
                Mol Biol Rep
                Molecular Biology Reports
                Springer Netherlands (Dordrecht )
                0301-4851
                1573-4978
                11 May 2011
                11 May 2011
                February 2012
                : 39
                : 2
                : 825-829
                Affiliations
                [1 ]Obesity Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, 19395-4763, Tehran, Iran
                [2 ]Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
                Article
                804
                10.1007/s11033-011-0804-4
                3249554
                21559831
                2fadeaec-401c-4f1e-9759-54605b110d2f
                © The Author(s) 2011
                History
                : 14 August 2010
                : 29 April 2011
                Categories
                Article
                Custom metadata
                © Springer Science+Business Media B.V. 2012

                Molecular biology
                bmi,tnf-α,obesity,polymorphism
                Molecular biology
                bmi, tnf-α, obesity, polymorphism

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