Magnesium metabolism in health and disease
Nephrology Department, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina. International Urology and Nephrology
(Impact Factor: 1.52).
04/2009; 41(2):357-62. DOI: 10.1007/s11255-009-9548-7
Magnesium (Mg) is the main intracellular divalent cation, and under basal conditions the small intestine absorbs 30-50% of its intake. Normal serum Mg ranges between 1.7-2.3 mg/dl (0.75-0.95 mmol/l), at any age. Even though eighty percent of serum Mg is filtered at the glomerulus, only 3% of it is finally excreted in the urine. Altered magnesium balance can be found in diabetes mellitus, chronic renal failure, nephrolithiasis, osteoporosis, aplastic osteopathy, and heart and vascular disease. Three physiopathologic mechanisms can induce Mg deficiency: reduced intestinal absorption, increased urinary losses, or intracellular shift of this cation. Intravenous or oral Mg repletion is the main treatment, and potassium-sparing diuretics may also induce renal Mg saving. Because the kidney has a very large capacity for Mg excretion, hypermagnesemia usually occurs in the setting of renal insufficiency and excessive Mg intake. Body excretion of Mg can be enhanced by use of saline diuresis, furosemide, or dialysis depending on the clinical situation.
Available from: Bing Zhou
- "It is of critical importance for various metabolic reactions, including energy production , protein and nucleic acid synthesis, cell cycle regulation and ion metabolism . Mg 2+ is closely related to many important human diseases such as type 2 diabetes mellitus, hypertension and cardiovascular diseases   . "
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ABSTRACT: The homeostasis of magnesium (Mg(2+)), an abundant divalent cation indispensable for many biological processes including mitochondrial functions, is underexplored. In yeast, the mitochondrial Mg(2+) homeostasis is accurately controlled through the combined effects of importers, Mrs2 and Lpe10, and an exporter, Mme1. However, little is known about this Mg(2+) homeostatic process in multicellular organisms. Here, we identified the first mitochondrial Mg(2+) transporter in Drosophila, the orthologue of yeast Mme1, dMme1, by homologous comparison and functional complementation. dMme1 can mediate the exportation of mitochondrial Mg(2+) when heterologously expressed in yeast. Altering the expression of dMme1, although only resulting in about a 10% change in mitochondrial Mg(2+) levels in either direction, led to a significant survival reduction in Drosophila. Furthermore, the reduced survival resulting from dMme1 expression changes could be completely rescued by feeding the dMME1-RNAi flies Mg(2+)-restricted food or the dMME1-over-expressing flies the Mg(2+)-supplemented diet. Our studies therefore identified the first Drosophila mitochondrial Mg(2+) exporter, which is involved in the precise control of mitochondrial Mg(2+) homeostasis to ensure an optimal state for survival.
Biochimica et Biophysica Acta 10/2015; 1863(1). DOI:10.1016/j.bbamcr.2015.10.004 · 4.66 Impact Factor
Available from: Abayomi O. Ige
- "Magnesium homeostasis is largely controlled by the kidneys which excrete about 120mg of magnesium into the urine per day (Rude, 2010). Though studies suggest that magnesium supplementation is generally non-toxic provided normal kidney function is maintained (Musso, 2009), there is however a dearth of information on haematological and serum biochemical changes that may occur due to oral magnesium supplementation. In addition, the glucose stabilizing effect of magnesium is widely reported but its effect on liver glycogen content is unclear. "
Available from: Bing Zhou
- "Mg 2+ also plays an important role in sustaining genomic stability and preventing carcinogenicity . Therefore, it is quite apprehensible that alterations in Mg 2+ metabolism would correlate to many important human diseases , including metabolic syndromes such as type 2 diabetes mellitus and hypertension . In higher plants, Mg 2+ also plays a critical role in regulating the chloroplast mRNA stability . "
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ABSTRACT: The homeostasis of magnesium (Mg(2+)), an abundant divalent cation indispensable for many biological processes including mitochondrial functions, is underexplored. Previously two mitochondrial Mg(2+) importers, Mrs2 and Lpe10, were characterized for mitochondrial Mg(2+) uptake. We now show that the mitochondrial Mg(2+) homeostasis is accurately controlled through the combined effects of previously known importers and a novel exporter, Mme1 (mitochondrial magnesium exporter 1). Mme1 belongs to the mitochondrial carrier family and was isolated for its mutation that is able to suppress the mrs2Δ respiration defect. Deletion of MME1 significantly increased the steady-state mitochondrial Mg(2+) concentration, while overexpression decreased it. Measurements of Mg(2+) exit from proteoliposomes reconstituted with purified Mme1 provided definite evidence for Mme1 as an Mg(2+) exporter. Our studies identified, for the first time, a mitochondrial Mg(2+) exporter that works together with mitochondrial importers to ensure a precise control of mitochondrial Mg(2+) homeostasis.
Copyright © 2015. Published by Elsevier B.V.
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 01/2015; 1853(3). DOI:10.1016/j.bbamcr.2014.12.029 · 5.02 Impact Factor
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