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FTO 基因变异 rs9939609 和 rs1421085 与成年人肥胖中糖和脂肪摄入增加的关联。

Association of FTO variants rs9939609 and rs1421085 with elevated sugar and fat consumption in adult obesity.

机构信息

Department of Tropical Nutrition and Food Science, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand.

Department of Molecular Tropical Medicine and Genetics, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand.

出版信息

Sci Rep. 2024 Oct 27;14(1):25618. doi: 10.1038/s41598-024-77004-6.

Abstract

This cross-sectional study explores the impact of FTO gene single nucleotide polymorphisms (SNPs) rs9939609 and rs1421085 on dietary habits contributing to obesity risk in Thai adults. The study enrolled 384 participants from Bangkok, categorized as non-obese (BMI < 25 kg/m) or obese (BMI ≥ 25 kg/m) based on WHO Asia Pacific Guidelines. Genotyping for FTO variants was performed using DNA from blood samples. While both SNPs adhered to Hardy-Weinberg equilibrium, the association between risk alleles and anthropometric measurements was not statistically significant. However, risk allele carriers showed significantly higher intakes of sugar and saturated fat compared to homozygous dominant individuals. In the obese group, the odds ratio for high-sugar intake was 2.22 (95% CI 1.13-4.37, p = 0.021) for rs9939609 risk allele carriers. For high-saturated fat intake, the odds ratio was 1.86 (95% CI 1.02-3.40, p = 0.041). Similar associations were observed for rs1421085. Risk allele carriers also exhibited significantly higher leptin levels (p < 0.043) and a positive correlation with myeloperoxidase levels (p < 0.038). These findings highlight the complex relationship between FTO risk alleles, increased consumption of sugar and saturated fat, and obesity-related parameters. The insights emphasize the importance of considering both genetic and dietary factors in obesity prevention strategies.

摘要

本横断面研究旨在探讨 FTO 基因单核苷酸多态性(SNP)rs9939609 和 rs1421085 对导致泰国成年人肥胖风险的饮食习惯的影响。该研究共纳入了 384 名来自曼谷的参与者,根据世界卫生组织亚太地区指南,将他们分为非肥胖组(BMI<25kg/m2)和肥胖组(BMI≥25kg/m2)。使用来自血液样本的 DNA 对 FTO 变体进行基因分型。虽然两个 SNP 均符合 Hardy-Weinberg 平衡,但风险等位基因与人体测量学指标之间的关联没有统计学意义。然而,与纯合显性个体相比,风险等位基因携带者的糖和饱和脂肪摄入量显著更高。在肥胖组中,rs9939609 风险等位基因携带者高糖摄入量的比值比为 2.22(95%置信区间为 1.13-4.37,p=0.021)。对于高饱和脂肪摄入量,比值比为 1.86(95%置信区间为 1.02-3.40,p=0.041)。rs1421085 也观察到了类似的关联。风险等位基因携带者的瘦素水平也显著升高(p<0.043),并且与髓过氧化物酶水平呈正相关(p<0.038)。这些发现强调了 FTO 风险等位基因、糖和饱和脂肪摄入增加与肥胖相关参数之间复杂的关系。这些研究结果强调了在肥胖预防策略中同时考虑遗传和饮食因素的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a17/11514288/6c2516217d24/41598_2024_77004_Fig1_HTML.jpg

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