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Open Access Research article

The G-308A variant of the Tumor Necrosis Factor-α (TNF-α) gene is not associated with obesity, insulin resistance and body fat distribution

Stefano Romeo1, Federica Sentinelli1, Francesca Capici1, Marcello Arca2, Andrea Berni3, Elio Vecci1, Umberto Di Mario1 and Marco Giorgio Baroni1*

Author Affiliations

1 Department of Clinical Science, Division of Endocrinology, University of Rome "La Sapienza", Rome, 00161, Italy

2 Institute of Terapia Medica Sistematica, University of Rome "La Sapienza", Rome, 00161, Italy

3 Institute of Heart Surgery, Cardiac Catheterisation Laboratories, University of Rome "La Sapienza", Rome, 00161, Italy

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BMC Medical Genetics 2001, 2:10  doi:10.1186/1471-2350-2-10

Published: 7 September 2001

Abstract

Background

Tumor Necrosis Factor-α (TNF-α) has been implicated in the pathogenesis of insulin resistance and obesity. The increased expression of TNF-α in adipose tissue has been shown to induce insulin resistance, and a polymorphism at position -308 in the promoter region ofTNF-α has been shown to increase transcription of the gene in adipocytes. Aim of this study is to investigate the role of the G-308A TNFα variant in obesity and to study the possible influence of this mutation on body fat distribution and on measures of obesity (including Fat Free Mass, Fat Mass, basal metabolic rate), insulin resistance (measured as HOMAIR), and lipid abnormalities. The G-308A TNFα polymorphism has been studied in 115 patients with obesity (mean BMI 33.9 ± 0.5) and in 79 normal lean subjects (mean BMI 24.3 ± 0.3).

Methods

The G-308A variant, detected by PCR amplification and Nco-1 digestion, determines the loss of a restriction site resulting in a single band of 107 bp [the (A) allele].

Results

The (A) allele frequencies of the G-308A TNFα polymorphism were 13.1% in the obese group and 14.6% in the lean subjects, with no significant difference between the two groups. Furthermore, no association was found with BMI classes, body fat distribution, HOMAIR, and metabolic abnormalities.

Conclusions

Our study did not detect any significant association of the G-308A TNFα polymorphism with obesity or with its clinical and metabolic abnormalities in this population. Our data suggests that, in our population, the G-308A TNFα polymorphism is unlikely to play a major role in the pathogenesis of these conditions.