Rayssiguier Y, Gueux E, Nowacki W, Rock E, Mazur A
INRA, Unité de Nutrition Humaine, Clermont Ferrand/Theix, 63122 Saint-Genès-Champanelle, France.
Magnes Res. 2006 Dec;19(4):237-43.
The metabolic syndrome is a cluster of common pathologies: abdominal obesity linked to an excess of visceral fat, insulin resistance, dyslipidemia and hypertension. This syndrome is occurring at epidemic rates, with dramatic consequences for human health worldwide, and appears to have emerged largely from changes in our diet and reduced physical activity. An important but not well-appreciated dietary change has been the substantial increase in fructose intake, which appears to be an important causative factor in the metabolic syndrome. There is also experimental and clinical evidence that the amount of magnesium in the western diet is insufficient to meet individual needs and that magnesium deficiency may contribute to insulin resistance. In recent years, several studies have been published that implicate subclinical chronic inflammation as an important pathogenic factor in the development of metabolic syndrome. Pro-inflammatory molecules produced by adipose tissue have been implicated in the development of insulin resistance. The present review will discuss experimental evidence showing that the metabolic syndrome, high fructose intake and low magnesium diet may all be linked to the inflammatory response. In many ways, fructose-fed rats display the changes observed in the metabolic syndrome and recent studies indicate that high-fructose feeding is associated with NADPH oxidase and renin-angiotensin activation. The production of reactive oxygen species results in the initiation and development of insulin resistance, hyperlipemia and high blood pressure in this model. In this rat model, a few days of experimental magnesium deficiency produces a clinical inflammatory syndrome characterized by leukocyte and macrophage activation, release of inflammatory cytokines, appearance of the acute phase proteins and excessive production of free radicals. Because magnesium acts as a natural calcium antagonist, the molecular basis for the inflammatory response is probably the result of a modulation of the intracellular calcium concentration. Potential mechanisms include the priming of phagocytic cells, the opening of calcium channels, activation of N-methyl-D-aspartate (NMDA) receptors, the activation of nuclear factor-kappaB (NFkB) and activation of the renin-angiotensin system. Since magnesium deficiency has a pro-inflammatory effect, the expected consequence would be an increased risk of developing insulin resistance when magnesium deficiency is combined with a high-fructose diet. Accordingly, magnesium deficiency combined with a high-fructose diet induces insulin resistance, hypertension, dyslipidemia, endothelial activation and prothrombic changes in combination with the upregulation of markers of inflammation and oxidative stress.
与内脏脂肪过多相关的腹部肥胖、胰岛素抵抗、血脂异常和高血压。这种综合征正以流行的速度出现，对全球人类健康产生了巨大影响，而且似乎很大程度上源于我们饮食的变化和体力活动的减少。果糖摄入量的大幅增加是一个重要但未得到充分认识的饮食变化，这似乎是代谢综合征的一个重要致病因素。此外，有实验和临床证据表明，西方饮食中的镁含量不足以满足个体需求，镁缺乏可能导致胰岛素抵抗。近年来，有几项研究表明亚临床慢性炎症是代谢综合征发展的一个重要致病因素。脂肪组织产生的促炎分子与胰岛素抵抗的发展有关。本综述将讨论实验证据，表明代谢综合征、高果糖摄入和低镁饮食可能都与炎症反应有关。在许多方面，喂食果糖的大鼠表现出代谢综合征中观察到的变化，最近的研究表明，高果糖喂养与NADPH氧化酶和肾素 - 血管紧张素激活有关。活性氧的产生导致该模型中胰岛素抵抗、高脂血症和高血压的发生和发展。在这个大鼠模型中，几天的实验性镁缺乏会产生一种临床炎症综合征，其特征为白细胞和巨噬细胞激活、炎症细胞因子释放、急性期蛋白出现以及自由基过度产生。由于镁作为天然的钙拮抗剂，炎症反应的分子基础可能是细胞内钙浓度调节的结果。潜在机制包括吞噬细胞的启动、钙通道的开放、N - 甲基 - D - 天冬氨酸（NMDA）受体的激活、核因子 - κB（NFkB）的激活以及肾素 - 血管紧张素系统的激活。由于镁缺乏具有促炎作用，当镁缺乏与高果糖饮食相结合时，预期结果将是发生胰岛素抵抗的风险增加。因此，镁缺乏与高果糖饮食相结合会导致胰岛素抵抗、高血压、血脂异常、内皮激活和血栓前状态的改变，并伴有炎症和氧化应激标志物的上调。
