Key result
LPA rs10455872 polymorphism distribution does not differ between children with obesity and healthy controls.
Why the study?
Genetic polymorphisms of the LPA gene may influence susceptibility to obesity, but the role of the LPA rs10455872 polymorphism in childhood obesity risk and clinical phenotypes was not well defined.
Is the LPA rs10455872 polymorphism associated with the risk and clinical phenotypes of childhood obesity?
Case-Control (n=180)
Is the LPA rs10455872 polymorphism associated with the risk and clinical phenotypes of childhood obesity?
p-value: p=0.563
The LPA rs10455872 polymorphism does not significantly affect the risk of childhood obesity but may be associated with differences in metabolic markers like vitamin B12 among obese children.
No link to childhood obesity risk in case-control data; leaves open metabolic phenotype associations for prospective study.
Background/Objectives: Obesity is associated with cardiovascular disease worldwide. An increased lipoprotein A (LpA) level is an independent risk factor for cardiovascular disease in children. Genetic polymorphisms of the LPA gene may play an important role in susceptibility to obesity. The aim of this study was to investigate the association of LPA rs10455872 polymorphism with the risk and clinical phenotypes of childhood obesity. Methods: This study included 103 children with obesity and 77 healthy controls. Genotyping of the LPA rs10455872 polymorphism was performed using real-time PCR. Results: The genotype distributions of the LPA rs10455872 polymorphism did not differ significantly between children with obesity and healthy children (p = 0.563). A marked difference in insulin levels was observed between children with obesity carrying the AG (16.90 IU/mL) and AA (25.57 IU/mL) genotypes. A marked difference was also observed in CRP levels between children with obesity with the AG (2.31 mg/L) and AA (4.25 mg/L) genotypes. After correcting for multiple comparisons using the false discovery rate (FDR), significant differences were found between AG and AA genotypes in vitamin B12 (adjusted p = 0.024). Serum iron showed a borderline association (adjusted p = 0.072). A statistically significant correlation was found between the metabolic syndrome index and body fat ratio among children with obesity with the AA genotype (p = 0.028). Conclusions: Although limited by the small number of children with obesity with the AG genotype, some differences were noted between the AG and AA genotypes. These exploratory findings require further investigation in adequately powered studies. In children with obesity with the AA genotype, the metabolic syndrome index increases as the body fat ratio increases.
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Haksayar et al. (2025) conducted a case-control in Childhood obesity (n=180). LPA rs10455872 polymorphism vs. Healthy controls was evaluated on Genotype distributions of the LPA rs10455872 polymorphism between children with obesity and healthy children (p=0.563). The LPA rs10455872 polymorphism genotype distribution did not differ significantly between children with obesity and healthy controls (p=0.563).
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