Tufts University Friedman School of Nutrition Science and Policy, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA.
J Nutr. 2013 Mar;143(3):345-53. doi: 10.3945/jn.112.172049. Epub 2013 Jan 23.
Favorable associations between magnesium intake and glycemic traits, such as fasting glucose and insulin, are observed in observational and clinical studies, but whether genetic variation affects these associations is largely unknown. We hypothesized that single nucleotide polymorphisms (SNPs) associated with either glycemic traits or magnesium metabolism affect the association between magnesium intake and fasting glucose and insulin. Fifteen studies from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) Consortium provided data from up to 52,684 participants of European descent without known diabetes. In fixed-effects meta-analyses, we quantified 1) cross-sectional associations of dietary magnesium intake with fasting glucose (mmol/L) and insulin (ln-pmol/L) and 2) interactions between magnesium intake and SNPs related to fasting glucose (16 SNPs), insulin (2 SNPs), or magnesium (8 SNPs) on fasting glucose and insulin. After adjustment for age, sex, energy intake, BMI, and behavioral risk factors, magnesium (per 50-mg/d increment) was inversely associated with fasting glucose [β = -0.009 mmol/L (95% CI: -0.013, -0.005), P < 0.0001] and insulin [-0.020 ln-pmol/L (95% CI: -0.024, -0.017), P < 0.0001]. No magnesium-related SNP or interaction between any SNP and magnesium reached significance after correction for multiple testing. However, rs2274924 in magnesium transporter-encoding TRPM6 showed a nominal association (uncorrected P = 0.03) with glucose, and rs11558471 in SLC30A8 and rs3740393 near CNNM2 showed a nominal interaction (uncorrected, both P = 0.02) with magnesium on glucose. Consistent with other studies, a higher magnesium intake was associated with lower fasting glucose and insulin. Nominal evidence of TRPM6 influence and magnesium interaction with select loci suggests that further investigation is warranted.
镁摄入量与血糖特征(如空腹血糖和胰岛素)之间存在有利关联,这在观察性和临床研究中得到了证实,但遗传变异是否会影响这些关联尚不清楚。我们假设,与血糖特征或镁代谢相关的单核苷酸多态性(SNP)会影响镁摄入量与空腹血糖和胰岛素之间的关联。来自遗传与人口健康领域的大型国际合作项目(CHARGE)联盟的 15 项研究提供了来自 52684 名无已知糖尿病的欧洲血统参与者的数据。在固定效应荟萃分析中,我们量化了 1)饮食镁摄入量与空腹血糖(mmol/L)和胰岛素(ln-pmol/L)的横断面关联,以及 2)镁摄入量与与空腹血糖(16 个 SNP)、胰岛素(2 个 SNP)或镁(8 个 SNP)相关的 SNP 之间的相互作用。在调整年龄、性别、能量摄入、BMI 和行为危险因素后,镁(每 50mg/d 增量)与空腹血糖呈负相关[β = -0.009mmol/L(95%CI:-0.013,-0.005),P < 0.0001]和胰岛素[-0.020ln-pmol/L(95%CI:-0.024,-0.017),P < 0.0001]。经过多次测试校正后,没有发现与镁相关的 SNP 或任何 SNP 与镁之间的相互作用具有统计学意义。然而,镁转运蛋白编码基因 TRPM6 中的 rs2274924 与血糖呈名义关联(未经校正的 P = 0.03),SLC30A8 中的 rs11558471 和 CNNM2 附近的 rs3740393 与镁在血糖方面呈名义交互作用(未经校正,两者 P = 0.02)。与其他研究一致,较高的镁摄入量与较低的空腹血糖和胰岛素有关。TRPM6 影响和镁与特定基因座相互作用的名义证据表明,进一步的研究是必要的。