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rs1042713与肥胖及肥胖相关表型的关联及其在调节马来西亚成年人血糖指数中与膳食脂肪的相互作用

Association of rs1042713 with Obesity and Obesity-Related Phenotypes and Its Interaction with Dietary Fat in Modulating Glycaemic Indices in Malaysian Adults.

作者信息

Mitra Soma Roy, Tan Pui Yee, Amini Farahnaz

机构信息

School of Biosciences, Faculty of Science, University of Nottingham Malaysia Campus, Semenyih, Malaysia.

School of Healthy Aging, Medical Aesthetics & Regenerative Medicine, UCSI University, KL Campus, Kuala Lumpur, Malaysia.

出版信息

J Nutr Metab. 2019 Mar 17;2019:8718795. doi: 10.1155/2019/8718795. eCollection 2019.

DOI:10.1155/2019/8718795
PMID:31007954
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6441509/
Abstract

Gene-diet interaction studies have reported that individual variations in phenotypic traits may be due to variations in individual diet. Our study aimed to evaluate (i) the association of rs1042713 with obesity and obesity-related metabolic parameters and (ii) the effect of dietary nutrients on these associations in Malaysian adults. genotyping, dietary, physical activity, anthropometric, and biochemical data were collected from 79 obese and 99 nonobese individuals. Logistic regression revealed no association between rs1042713 and obesity (=0.725). However, the carriers of G allele (AG + GG genotypes) of rs1042713 were associated with increased odds of insulin resistance, 2.83 (CI = 1.04-7.70, adjusted =0.042), in the dominant model, even after adjusting for potential confounders. Obese individuals carrying the G allele were associated with higher total cholesterol (=0.011), LDL cholesterol levels (=0.008), and total cholesterol/HDL cholesterol ratio (=0.048), compared to the noncarriers (AA), even after adjusting for potential confounders. Irrespective of obesity, the carriers of GG genotype had significantly lower fasting glucose levels with low saturated fatty acid intake (<7.3% of TE/day) (4.92 ± 0.1 mmol/L vs 5.80 ± 0.3 mmol/L, =0.011) and high intake of polyunsaturated fatty acid:saturated fatty acid ratio (≥0.8/day) (4.83 ± 0.1 mmol/L vs 5.93 ± 0.4 mmol/L, =0.006). Moreover, the carriers of GG genotype with high polyunsaturated fatty acid intake (≥6% of TE/day) had significantly lower HOMA-IR (1.5 ± 0.3 vs 3.0 ± 0.7, =0.026) and fasting insulin levels (6.8 ± 1.6 U/mL vs 11.4 ± 2.1 U/mL, =0.036). These effects were not found in the noncarriers (AA). In conclusion, G allele carriers of rs1042713 were associated with increased odds of insulin resistance. Obese individuals carrying G allele were compromised with higher blood lipid levels. Although it is premature to report gene-diet interaction on the regulation of glucose and insulin levels in Malaysians, we suggest that higher quantity of PUFA-rich food sources in regular diet may benefit overweight and obese Malaysian adults metabolically. Large-scale studies are required to replicate and confirm the current findings in the Malaysian population.

摘要

基因-饮食相互作用研究表明,表型特征的个体差异可能归因于个体饮食的差异。我们的研究旨在评估:(i)rs1042713与肥胖及肥胖相关代谢参数之间的关联;(ii)膳食营养素对马来西亚成年人中这些关联的影响。我们收集了79名肥胖个体和99名非肥胖个体的基因分型、饮食、身体活动、人体测量及生化数据。逻辑回归分析显示rs1042713与肥胖之间无关联(P = 0.725)。然而,在显性模型中,即使校正了潜在混杂因素后,rs1042713的G等位基因携带者(AG + GG基因型)与胰岛素抵抗几率增加相关,比值比为2.83(95%置信区间 = 1.04 - 7.70,校正后P = 0.042)。与非携带者(AA)相比,即使校正了潜在混杂因素后,携带G等位基因的肥胖个体总胆固醇水平(P = 0.011)、低密度脂蛋白胆固醇水平(P = 0.008)及总胆固醇/高密度脂蛋白胆固醇比值(P = 0.048)更高。无论是否肥胖,GG基因型携带者在饱和脂肪酸摄入量低(<每日总能量的7.3%)时空腹血糖水平显著更低(4.92 ± 0.1 mmol/L对5.80 ± 0.3 mmol/L,P = 0.011),且在多不饱和脂肪酸:饱和脂肪酸比值高(≥0.8/天)时也是如此(4.83 ± 0.1 mmol/L对5.93 ± 0.4 mmol/L,P = 0.006)。此外,多不饱和脂肪酸摄入量高(≥每日总能量的6%)的GG基因型携带者稳态模型评估的胰岛素抵抗指数(HOMA-IR)显著更低(1.5 ± 0.3对3.0 ± 0.7,P = 0.026),空腹胰岛素水平也更低(6.8 ± 1.6 U/mL对11.4 ± 2.1 U/mL,P = 0.036)。在非携带者(AA)中未发现这些效应。总之,rs1042713的G等位基因携带者与胰岛素抵抗几率增加相关。携带G等位基因的肥胖个体血脂水平更高且代谢受损。尽管在马来西亚人中报告基因-饮食相互作用对葡萄糖和胰岛素水平的调节作用还为时过早,但我们建议在日常饮食中增加富含多不饱和脂肪酸食物的摄入量可能对超重和肥胖的马来西亚成年人的代谢有益。需要大规模研究来重复并确认马来西亚人群中的当前研究结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec5f/6441509/8e741cd6979d/JNME2019-8718795.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec5f/6441509/0fdd78f0281b/JNME2019-8718795.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec5f/6441509/8e741cd6979d/JNME2019-8718795.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec5f/6441509/0fdd78f0281b/JNME2019-8718795.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec5f/6441509/8e741cd6979d/JNME2019-8718795.002.jpg

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