Abstract
More than two billion people around the world are overweight or obese. Even in apparently healthy people, obesity has a potent effect on their quality of life. Experimental data indicate the role of infectious agents in systemic inflammation, revealing a correlation between the dietary habits of people with obesity and the level of systemic inflammation mediators, serum lipid concentration, and hormonal and immune status. This study aimed to determine the association of immune response and lipid metabolism gene polymorphisms with the risk of obesity. This study included 560 Caucasian participants living in Western Siberia (Russian Federation). A total of 52 polymorphic sites in 20 genes were analyzed using the 5′ TaqMan nuclease assay. Four risk-associated polymorphic variants were discovered—two variants in immune response genes (IL6R rs2229238, OR = 1.92, 95% CI = 1.36–2.7, p = 0.0002 in the dominant model; IL18 rs1946518, OR = 1.45, 95% CI = 1.03–2.04, p = 0.033 in the over-dominant model) and two variants in lipid metabolism genes (LPA rs10455872, OR = 1.86, 95% CI = 1.07–3.21, p = 0.026 in the log-additive model; LEPR rs1137100, OR = 2.88, 95% CI = 1.52–5.46, p = 0.001 in the recessive model). Thus, polymorphisms in immune response and lipid metabolism genes are potentially associated with the modification of obesity risk in the Caucasian population.
Highlights
Despite specific public health policies targeting the obesity epidemic, more than two billion people around the world are overweight or obese [1]
Four single-nucleotide polymorphisms (SNPs) associated with an increased risk of obesity were discovered—two variants in immune response genes (IL6R rs2229238, odds ratio (OR) = 1.92, 95% confidence interval (CI) = 1.36–2.7, p = 0.0002 in the dominant model; IL18 rs1946518, OR = 1.45, 95% CI = 1.03–2.04, p = 0.033 in the overdominant model) and two variants in lipid metabolism genes (LPA rs10455872, OR = 1.86, 95% CI = 1.07–3.21, p = 0.026 in the log-additive model; LEPR rs1137100, OR = 2.88, 95% CI = 1.52–5.46, p = 0.001 in the recessive model)
It was inferred that the A/A genotype of the TNF gene was associated with a high risk of presenting an obesity phenotype (OR = 10.29, 95% CI 1.22–86.59, p = 0.0081)
Summary
Despite specific public health policies targeting the obesity epidemic, more than two billion people around the world are overweight or obese [1]. Obesity is a multifactorial disease characterized by excessive accumulation of adipose tissue, accompanied by a low-grade chronic inflammation. The triggers of this inflammation are poorly studied, but it is known that the degree of inflammation correlates with the severity of obesity-associated pathologies, which suggests that understanding the inflammatory response may improve the treatment strategies of such diseases [3,4]. Despite the previously obtained results, some issues related to the genetics of obesity, including the role of SNPs in genes involved in the inflammation and lipid metabolism pathways mediating obesity, are still poorly investigated, and the available results are contradictory. Understanding the role of genetic factors controlling the different pathways underlying the pathogenesis of obesity, inflammation and lipid metabolism, plays a very important role in the development of personalized prevention strategies, especially in at-risk groups
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