Key result
TNFα and PTPN22 polymorphisms show no association with obesity risk.
Why the study?
Polymorphisms in the TNFα and PTPN22 genes increase the risk of immune and inflammatory diseases, and this study aimed to analyze biochemical parameters and the effect of TNFα -308G/A and PTPN22 +1858C/T polymorphisms on obesity susceptibility in adolescents.
Cross-Sectional (n=253)
No
Answers are grounded in this paper and cite their sources.
Observational analysis reveals no link between TNFα and PTPN22 polymorphisms and adolescent obesity risk, indicating altered metabolic markers in CT carriers.
Obesity is currently considered an inflammatory condition associated with autoimmune diseases, suggesting a common origin. Among other factors, candidate genes may explain the development of this disease. Polymorphisms in the tumor necrosis factor α (TNFα) and lymphoid protein tyrosine phosphatase (PTPN22) genes lead to an increased risk to development of immune and inflammatory diseases. The aim of the present study was to analyze the biochemical parameters and the effect of the TNFα -308G/A and PTPN22 +1858C/T polymorphisms in the susceptibility of adolescents to obesity. A group of 253 adolescent subjects were recruited and classified as obese, overweight or normal weight according to their nutritional status. Anthropometric measurements, clinical and biochemical data were analyzed. DNA was extracted from peripheral blood samples by the phenol-chloroform method, and TNFα -308G/A and PTPN22 1858C/T polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism assays. Clinical, genetic and biochemical parameters were analyzed to determine the existence of a possible association with the development of obesity. Statistically significant differences in body mass index, insulin, triglyceride levels and homeostatic model assessment for insulin resistance (HOMA-IR) index were observed among the three groups analyzed (P≤0.05). The studied polymorphisms did not confer a risk for developing obesity in the analyzed population (P>0.05); however, significantly low levels of insulin and decreased rates of HOMA-IR were observed in the 1858 CT genotype carriers of the PTPN22 gene. In conclusion, no association between the TNFα -308G/A and PTPN22 +1858C/T polymorphisms and the risk to development of obesity in the adolescent population analyzed was observed. However, the 1858 CT genotype of the PTPN22 gene was associated with variations of certain biochemical parameters analyzed.
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Salinas-Santander et al. (2015) conducted a cross-sectional in Obesity (n=253). TNFα -308G/A and PTPN22 +1858C/T gene polymorphisms vs. Wild-type genotypes (TNFα -308 GG and PTPN22 +1858 CC) was evaluated on Susceptibility to overweight and obesity (p=>0.05). TNFα -308G/A and PTPN22 +1858C/T polymorphisms were not associated with obesity risk, though PTPN22 1858 CT carriers had lower insulin and HOMA-IR.
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