Magnesium metabolism in health and disease
ABSTRACT 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.
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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 · 5.30 Impact Factor
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ABSTRACT: The present study compares blood plasma clinical-chemical parameters (BCCPs) in birds from three geographically distinct North Atlantic Great skua (Stercorarius skua) colonies. Birds from these sites bioaccumulate different POP (persistent organic pollutant) concentrations and that enabled us to compare Great skua BCCPs in different exposure scenarios. Persistent organic pollutants (organochlorines: PCB, DDT, chlordanes, HCB, HCH, mirex and brominated flame retardants: PBDEs) and nineteen BCCPs were analysed in 114 adult Great skuas sampled during summer 2009 in North Atlantic colonies at Bjørnøya (n=42), Iceland (n=57) and Shetland (n=15). Specimens from Bjørnøya had the highest blood plasma concentrations of all contaminant groups followed by Iceland and Shetland birds, respectively (ANOVA: p<0.05). Most of the 19 BCCP parameters followed the pattern of colony differences found for contaminants, with Bjørnøya having the highest concentrations. However seven BCCPs, the three liver enzymes ALKP, ALAT and GGT as well as bile acids, cholesterol, sodium and potassium, did not differ between colonies (ANOVA: p>0.05). Therefore correlation analyses of these seven BCCPs vs. POPs were done on the combined colony data while the analyses of the remaining 12 BCCPs were carried out for each colony separately. The analyses of combined colony data showed that the blood plasma concentration of liver enzymes ALAT and GGT increased with increasing concentrations of ΣPBDE and ΣHCH, HCB and ΣCHL, respectively (all Pearson's p<0.05). In Great skuas from Shetland, the important osmotic transport protein albumin increased with increasing concentrations of ΣPCB and ΣDDT, while total blood plasma protein increased with ΣPCB, ΣDDT, ΣHCH and HCB concentrations (all Pearson's p<0.05). In both Bjørnøya and Iceland skuas, blood plasma pancreatic enzyme amylase decreased with increasing ΣHCH concentrations while the erythrocyte waste product total bilirubin in blood plasma increased with increasing ΣHCH and ΣPBDE concentrations in Iceland Great skuas (all Pearson's p<0.05). In Bjørnøya birds, blood plasma urea from protein metabolism (reflects kidney function) increased with increasing ΣPBDE concentrations (Pearson's p<0.05). Furthermore, a redundancy analysis showed that 10.6% of the variations in BCCPs could be explained by the variations in POP concentrations. Based on these results we suggest that liver and renal functions could be negatively affected by different POP compounds. It is, however, uncertain if the colony BCCP differences and their relationship to POP concentrations reflect health effects that could have an overall impact on the populations via reduced survival and reproduction parameters.Ecotoxicology and Environmental Safety 03/2013; DOI:10.1016/j.ecoenv.2013.02.012 · 2.48 Impact Factor
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ABSTRACT: The effects of magnesium supplementation on blood pressure (BP) have been studied for over 25 years and results have been inconsistent. Blood pressure reductions in randomized studies have varied from 12 mmHg reductions to no reduction. The objective of this pilot intervention was to investigate the effect of magnesium supplementation on systolic blood pressure whilst resting and during recovery from aerobic and resistance exercise and on performance. A further objective was to see whether the effect of a high vs low habitual dietary magnesium intake affected these results. Sixteen male volunteers were randomly assigned to either a 300 mg·d(-1) magnesium oxide supplementation (MO) or a control group (CG) for 14 days. Resting blood pressure (BP) and heart rate (HR) were measured before subjects performed a maximal 30 minute cycle, immediately followed by three x 5 second isometric bench press, both at baseline and after the intervention. Blood pressure and heart rate were recorded immediately post exercise and after five minutes recovery. A 3 day food diary was recorded for all subjects to measure dietary magnesium intake. At the end of the intervention, the supplemented group, had a reduction in mean resting systolic BP by 8.9 mmHg (115.125 ± 9.46 mmHg, p = 0.01) and post exercise by 13 mmHg (122.625 ± 9. 88 mmHg, p = 0.01). Recovery BP was 11.9 mmHg lower in the intervention group compared to control (p = 0.006) and HR decreased by 7 beats per minute in the experimental group (69.0 ± 11.6 bpm, p = 0. 02). Performance indicators did not change within and between the groups. Habitual dietary magnesium intake affected both resting and post exercise systolic BP and the subsequent effect of the magnesium supplementation. These results have an implication in a health setting and for health and exercise but not performance. Key pointsMagnesium supplementation will have an effect on resting and recovery systolic blood pressure with aerobic exercise.Magnesium supplementation will have an effect on resting and recovery systolic blood pressure with resistance exercise.Magnesium supplementation did not have an effect on performance indicators.A low habitual dietary magnesium intake will negatively affect blood pressure.A high habitual dietary magnesium intake will impact on the effect of magnesium supplementation.Journal of sports science & medicine 01/2013; 12(1):144-50. · 0.90 Impact Factor