Interactions of dietary whole-grain intake with fasting glucose- and insulin-related genetic loci in individuals of European descent: a meta-analysis of 14 cohort studies.
Interactions of dietary whole-grain intake with fasting glucose- and insulin-related genetic loci in individuals of European descent: a meta-analysis of 14 cohort studies.
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DOI：
10.2337/dc10-1150
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发表时间：
2010-12
期刊：
影响因子：
16.2
通讯作者：
Meigs JB
中科院分区：
文献类型：
--
作者：
Nettleton JA;McKeown NM;Kanoni S;Lemaitre RN;Hivert MF;Ngwa J;van Rooij FJ;Sonestedt E;Wojczynski MK;Ye Z;Tanaka T;Garcia M;Anderson JS;Follis JL;Djousse L;Mukamal K;Papoutsakis C;Mozaffarian D;Zillikens MC;Bandinelli S;Bennett AJ;Borecki IB;Feitosa MF;Ferrucci L;Forouhi NG;Groves CJ;Hallmans G;Harris T;Hofman A;Houston DK;Hu FB;Johansson I;Kritchevsky SB;Langenberg C;Launer L;Liu Y;Loos RJ;Nalls M;Orho-Melander M;Renstrom F;Rice K;Riserus U;Rolandsson O;Rotter JI;Saylor G;Sijbrands EJ;Sjogren P;Smith A;Steingrímsdóttir L;Uitterlinden AG;Wareham NJ;Prokopenko I;Pankow JS;van Duijn CM;Florez JC;Witteman JC;MAGIC Investigators;Dupuis J;Dedoussis GV;Ordovas JM;Ingelsson E;Cupples L;Siscovick DS;Franks PW;Meigs JB
全谷物食品被吹捧为多种健康益处，包括增强胰岛素敏感性和降低2型糖尿病风险。最近的全基因组关联研究（GWAS）已经确定了几个单核苷酸多态性（SNP）与空腹血糖和胰岛素浓度在个人的糖尿病。我们检验了全麦食物摄入和遗传变异相互作用影响空腹血糖和胰岛素浓度的假设。通过对来自14个队列（包括148，000名欧洲血统参与者）的数据进行荟萃分析，我们研究了全谷物摄入量与先前在GWAS中与空腹血糖（16个位点）和/或胰岛素（2个位点）浓度相关的位点的相互作用。对于相互作用的检验，我们认为P值<0.0028（18次检验中的0.05）具有统计学显著性。更多的全谷物食物摄入与较低的空腹血糖和胰岛素浓度相关，与人口统计学、其他饮食和生活方式因素以及BMI无关（β [95% CI]每1份多全谷物摄入量：−0.009 mmol/l葡萄糖[−0.013至−0.005]，P < 0.0001和−0.011 pmol/l [ln]胰岛素[−0.015至−0.007]，P = 0.0003）。没有相互作用达到我们的多重检验调整的统计学显著性阈值。与全谷物摄入量最强的SNP相互作用是空腹胰岛素的rs780094（GCKR）（P = 0.006），其中较大的全谷物摄入量与具有胰岛素升高等位基因的空腹胰岛素浓度的较小降低相关。我们的研究结果支持全谷物摄入量与空腹血糖和胰岛素的有利关联，并表明GCKR和全谷物摄入量的变化在影响空腹胰岛素浓度方面存在潜在的相互作用。
Whole-grain foods are touted for multiple health benefits, including enhancing insulin sensitivity and reducing type 2 diabetes risk. Recent genome-wide association studies (GWAS) have identified several single nucleotide polymorphisms (SNPs) associated with fasting glucose and insulin concentrations in individuals free of diabetes. We tested the hypothesis that whole-grain food intake and genetic variation interact to influence concentrations of fasting glucose and insulin. Via meta-analysis of data from 14 cohorts comprising ∼48,000 participants of European descent, we studied interactions of whole-grain intake with loci previously associated in GWAS with fasting glucose (16 loci) and/or insulin (2 loci) concentrations. For tests of interaction, we considered a P value <0.0028 (0.05 of 18 tests) as statistically significant. Greater whole-grain food intake was associated with lower fasting glucose and insulin concentrations independent of demographics, other dietary and lifestyle factors, and BMI (β [95% CI] per 1-serving-greater whole-grain intake: −0.009 mmol/l glucose [−0.013 to −0.005], P < 0.0001 and −0.011 pmol/l [ln] insulin [−0.015 to −0.007], P = 0.0003). No interactions met our multiple testing–adjusted statistical significance threshold. The strongest SNP interaction with whole-grain intake was rs780094 (GCKR) for fasting insulin (P = 0.006), where greater whole-grain intake was associated with a smaller reduction in fasting insulin concentrations in those with the insulin-raising allele. Our results support the favorable association of whole-grain intake with fasting glucose and insulin and suggest a potential interaction between variation in GCKR and whole-grain intake in influencing fasting insulin concentrations.
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