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The association of gene polymorphisms in SREBP and its interaction with nutritional status on blood pressure phenotypes among children: a cross-sectional study

Year: 2025

Type: article

Abstract: Previous studies have confirmed that the SREBP polymorphisms are associated with dyslipidemia. However, no researchers investigated the association between SREBP polymorphisms and blood pressure phenotypes in children. A convenient cluster sampling method was adopted to conduct field survey in three middle schools. A total of 872 children were included in this cross-sectional study final analysis. Matrix-supported laser release/ionization time-of-flight mass spectrometry was used for genotyping of SREBP polymorphism. The association between SREBP polymorphisms and blood pressure phenotypes was analyzed by multivariable linear regression and Logistic regression analysis. A Bonferroni-corrected threshold of P < 0.025 ( SREBP1 ) or P < 0.0125 ( SREBP2 ) was considered significant. After adjusting for age, sex, age squared and BMI, individuals with GA/AA genotype of SREBP1 /rs11868035 had higher systolic blood pressure (SBP) ( β = 7.34, P = 0.004) than GG genotype, and SREBP1 /rs2297508 C allele carriers were positively associated with SBP (β = 7.19, P = 0.008). A significant interaction between SREBP2 /rs2228314 and gender on the risk of High Blood Pressure (HBP) ( P interaction = 0.034) was found. In boys, HBP risk increased by 101% for each additional G allele ( OR = 2.01, 95% CI 1.15–3.53, P = 0.015), but not in girls. Besides, we also identified an interaction between SREBP2 /rs2267439 and nutritional status on the risk of HBP ( P interaction =0.023). The risk of HBP in SREBP2 /rs2267439 CT/TT genotype carriers is higher than that in CC genotype carriers in the overweight/obese children ( OR = 2.68, 95% CI 1.06–6.75, P = 0.036), but no in non-overweight/obese children. SREBP polymorphisms were significantly associated with blood pressure in children. It provides possible clues for personalized prevention and intervention of HBP in children from the perspective of genetic susceptibility.

Source: BMC Cardiovascular Disorders

DOI: 10.1186/s12872-025-05038-3