Corresponding author: Nicola M. McKeown,
Diabetes Care. 2014 Feb;37(2):419-27. doi: 10.2337/dc13-1397. Epub 2013 Oct 2.
To assess 7-year associations between magnesium intake and incident prediabetes and/or insulin resistance (IR), and progression from these states to type 2 diabetes.
In 2,582 community-dwelling participants 26-81 years old at baseline, magnesium intake and risk of incident "metabolic impairment," defined as impaired fasting glucose (FG) (≥5.6 to <7.0 mmol/L), impaired glucose tolerance (2-h postload glucose ≥7.8 to <11.1 mmol/L), IR, or hyperinsulinemia (≥90th percentile of homeostasis model assessment of IR or fasting insulin, respectively), was estimated among those with normal baseline status, and risk of incident diabetes was estimated among those with baseline metabolic impairment. In participants without incident diabetes, we examined magnesium intake in relation to 7-year changes in fasting and postload glucose and insulin, IR, and insulin sensitivity.
After adjusting for age, sex, and energy intake, compared with those with the lowest magnesium intake, those with the highest intake had 37% lower risk of incident metabolic impairment (P trend = 0.02), and in those with baseline metabolic impairment, higher intake was associated with 32% lower risk of incident diabetes (P trend = 0.05). In the combined population, the risk in those with the highest intake was 53% (P trend = 0.0004) of those with the lowest intake. Adjusting for risk factors and dietary fiber attenuated associations in the baseline normal population but did not substantially affect associations in the metabolically impaired. Higher magnesium intake tended to associate with lower follow-up FG and IR, but not fasting insulin, postload values, or insulin sensitivity.
Magnesium intake may be particularly beneficial in offsetting risk of developing diabetes among those at high risk. Magnesium's long-term associations with non-steady-state (dynamic) measures deserve further research.
评估镁摄入量与 7 年内发生前驱糖尿病和/或胰岛素抵抗(IR)的关联,以及这些状态向 2 型糖尿病进展的情况。
在 2582 名基线时年龄在 26-81 岁、居住在社区的参与者中,评估镁摄入量与新发“代谢损伤”(定义为空腹血糖受损(FG)(≥5.6 至<7.0mmol/L)、葡萄糖耐量受损(餐后 2 小时血糖≥7.8 至<11.1mmol/L)、IR 或高胰岛素血症(分别为 IR 和空腹胰岛素的稳态模型评估的第 90 百分位数或)的风险,在基线代谢损伤的参与者中评估新发糖尿病的风险。在没有新发糖尿病的参与者中,我们检查了镁摄入量与空腹和餐后血糖和胰岛素、IR 和胰岛素敏感性 7 年变化之间的关系。
在校正年龄、性别和能量摄入后,与镁摄入量最低的参与者相比,镁摄入量最高的参与者新发代谢损伤的风险降低了 37%(P 趋势=0.02),并且在基线代谢损伤的参与者中,较高的镁摄入量与新发糖尿病的风险降低了 32%(P 趋势=0.05)。在合并人群中,最高摄入量者的风险是最低摄入量者的 53%(P 趋势=0.0004)。在基线正常人群中,调整危险因素和膳食纤维会减弱关联,但在代谢受损人群中不会显著影响关联。较高的镁摄入量往往与较低的随访 FG 和 IR 相关,但与空腹胰岛素、餐后值或胰岛素敏感性无关。
镁摄入量可能特别有益于降低高危人群发生糖尿病的风险。镁与非稳态(动态)测量的长期关联值得进一步研究。