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Texte intégral de l'article
 
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Commentary to the letter to the editor


Magnesium Research. Volume 23, Numéro 3, september 2010, Letter to the editor

DOI : 10.1684/mrh.2010.0215


Auteur(s) : Yves Rayssiguier, Edmond Rock , Unité de Nutrition Humaine, INRA, Theix, France.

ARTICLE

Auteur(s) : Yves Rayssiguier, Edmond Rock

Unité de Nutrition Humaine, INRA, Theix, France

The letter from Günther [1] reminds us that magnesium deficiency leads to an increase of intracellular calcium which can contribute to hypertension and insulin resistance. Therefore the proposed “ionic hypothesis” can be considered as a potential mechanism underlying the metabolic syndrome. However, the paper concludes that magnesium deficiency would not be involved in insulin resistance and would not promote the metabolic syndrome. The author also quite rightly emphasises the need to distinguish the effects of hypomagnesemia from a decrease of intracellular magnesium on the blood pressure. Obesity is reported as a major risk factor for metabolic syndrome without referring to data recently published on the possible impact of dietary magnesium on metabolic syndrome. To mention that patients with mutations on mitochondrial transfer RNA also develop hypomagnesaemia, hypertension and hyperlipemia with neither obesity nor insulin resistance is not sufficient to exclude the involvement of magnesium in the development of metabolic syndrome. Based on recent studies, there is now strong plausibility for the impact of magnesium intake on cardiovascular disease factors and metabolic syndrome [2]. The effect of magnesium deficiency on the development of insulin resistance, alteration of blood pressure, atherogenic changes in lipoprotein metabolism and endothelial dysfunction are well documented in animal models. Moreover, experimental Mg deficiency induces a clinical inflammatory syndrome characterised by the synthesis of pro-inflammatory cytokines and extensive production of free radicals. An increase in the level of extracellular magnesium decreases the inflammatory syndrome, while a reduction of extracellular magnesium results in cell activation. Therefore, the concept that the metabolic syndrome is an inflammatory condition may explain the role of magnesium deficiency through its potential for inducing pro-inflammatory changes. Moreover, recent findings support the hypothesis that the effect of magnesium on intracellular calcium homeostasis may be a common link between stress, inflammation and the metabolic syndrome [3]. In humans, epidemiological studies have described an inverse relationship between magnesium-rich food intake and diabetes, insulin resistance and metabolic syndrome but also between Mg intake and markers of chronic inflammation. However, a limitation of observational studies linking dietary magnesium and metabolic syndrome is that that there is also a strong association between magnesium and other beneficial nutrients commonly found particularly in plant foods (phytochemicals, fibres, etc.) and insulin resistance itself may contribute to magnesium depletion. Given the fact that magnesium intake is often inadequate in the western diet, and that metabolic syndrome is highly prevalent in the population consuming that diet, the best current recommendation is to include magnesium-rich foods in the usual diet.

References

1 Günther T. Biochemical mechanisms of the metabolic syndrome and the role of magnesium. Magnes Res 2010; 23: 142-5.

2 Bo S, Pisu E. Role of dietary magnesium in cardiovascular disease prevention, insulin sensitivity and diabetes. Curr Opin Lipidol 2008; 19: 50-6.

3 Rayssiguier Y, Libako P, Nowacki W, Rock E. Magnesium deficiency and metabolic syndrome: stress and inflammation may reflect calcium activation. Magnes Res 2010; 23: 73-80.


 

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