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PubMed2006

Magnesium-deficient diet-induced reduction in protein utilization in rats is reversed by dietary magnesium supplementation.

We investigated the effect of dietary magnesium (Mg) level on protein utilization in rats. Male Wistar rats were fed a control diet (control group) and a Mg-deficient diet (Mg-deficient group) for 28 days. After 28 days, the diet of half of the Mg-deficient group (recovery group) was changed from the Mg-deficient diet to the control diet for either 7 or 14 days. After 28 days, final body weight, weight gain and food efficiency were significantly decreased due to the Mg-deficient diet. Apparent Mg absorption, Mg retention and serum Mg levels were also significantly decreased due to the Mg-deficient diet. Furthermore, the Mg-deficient group showed a significant increase in urinary nitrogen (N) excretion and significant decreases in N retention and serum albumin level. At day 7 and 14 after changing the Mg-deficient diet to the control diet, apparent Mg absorption, Mg retention and serum Mg levels were significantly increased in the recovery group as compared with those in the Mg-deficient group. However, with regard to final body weight, weight gain and food efficiency, no significant differences were observed between the Mg-deficient group and the recovery group. At day 14 after changing the diet, urinary N excretion was significantly decreased and N retention was significantly increased in the recovery group as compared with the Mg-deficient group. At day 7 and 14 after changing the diet, the serum albumin level was also significantly increased in the recovery group as compared with that in the Mg-deficient group. These results suggest that: 1) the Mg-deficient diet depresses protein utilization; 2) the Mg-deficient diet-induced impairment of protein utilization is reversed by dietary Mg supplementation; and 3) the Mg-deficient diet-induced growth retardation is not completely reversed after 14 days of Mg supplementation.

Animals↗
PubMedDate not supplied

Magnesium in primary care and preventive medicine: clinical correlation of magnesium loading studies.

Diagnostic categories that are useful for describing patients with acute or organ failure disease are generally less useful labels for primary care and preventive medicine patients whose conditions are better described by signs and symptoms. Symptoms may be clues to ill health but are not often criteria for a major diagnostic labeling. In my practice I have used a computer-based medical record system that permits portrayal and comparison of symptom data to correlate varying degrees of retention of an intramuscular magnesium-loading study (IMMLS) with symptom patterns in 172 patients. The group of patients who show a paradoxical excretion of more Mg than they were given in the IMMLS are a distinctive group with lower blood pressures and significantly fewer digestive and skin symptoms, fewer symptoms of inflammation but more emotional symptoms than those with normal Mg excretion. The group who retained > 49% of the load had higher blood pressures and significantly fewer symptoms of inflammation of the skin and of the reproductive tract.

Adolescent↗
PubMed1990

Effect of intravenous magnesium sulfate on blood magnesium parameters.

Magnesium sulfate was administered intravenously (0.6 mEq/kg body weight over 10 min) to 13 patients with hypertrophic cardiomyopathy undergoing electrophysiologic testing. Total serum, ultrafilterable and protein-bound serum, mononuclear blood cell (MBC) content and concentration, and red blood cell (RBC) concentration of Mg were measured at the following intervals: (1) baseline (before Mg infusion), (2) at the end of infusion, and (3) approximately 40 min after the end of infusion. The total serum, ultrafilterable, and protein-bound fractions rose immediately after infusion and fell by 40 min. The RBC Mg rose and fell less sharply than the serum parameters after Mg infusion. In contrast, the MBC Mg content continued to rise significantly at 40 min after Mg infusion, and MBC concentration showed a continued trend to rise, although this was not statistically significant.

Adult↗
PubMed1990

The liver glucose-6-phosphatase of intact microsomes is inhibited and displays sigmoid kinetics in the presence of alpha-ketoglutarate-magnesium and oxaloacetate-magnesium chelates.

We have recently shown that the Ca.EGTA and Mg.EDTA complexes, but not free Ca2+ or Mg2+, inhibit the liver glucose-6-phosphatase (Mithieux, G., Vega, F. V., Beylot, M., and Riou, J. P. (1990) J. Biol. Chem. 265, 7257-7259). In this work, we report that, when complexed with Mg2+, two endogenous dicarboxylic keto acids (alpha-ketoglutarate (alpha-KG) and oxaloacetate (OAA] inhibit the glucose-6-phosphatase activity at low concentrations of substrate. This phenomenon is specific for complexes of Mg2+ with alpha-KG and OAA since 1) the complexes of Mg2+ with a number of other di- or tricarboxylic acids having high structural analogy with alpha-KG and OAA (oxalate, malate, succinate, citrate, aspartate, and glutamate) do not inhibit the glucose-6-phosphatase activity and 2) the Ca.alpha-KG and Ca.OAA chelates do not inhibit the glucose-6-phosphatase activity. In the presence of Mg.alpha-KG or Mg.OAA chelates, the enzyme displays sigmoid kinetics; the Hanes plots deviate from linearity, indicating the positive cooperative dependence of the velocity upon the substrate concentration. Hill coefficients (equal to 1 in the absence of the chelates) of 1.23 and 1.33 have been determined in the presence of Mg.alpha-KG and Mg.OAA complexes, respectively. The disruption of microsomal integrity by detergents abolishes the effect of Mg.alpha-KG and Mg.OAA, suggesting that the magnesium chelates inhibit the translocase component of the glucose-6-phosphatase system.

Animals↗
PubMed1988

Availability of body magnesium during magnesium deficiency.

Extensive experimental and clinical studies in animals and humans during the past 25 years have yielded considerable data regarding the availability of internal magnesium (Mg) stores for the maintenance of extracellular and critical tissue concentrations of Mg during periods of Mg deprivation. The bulk of body Mg is present in bone and skeletal muscle, and it is these two sites that provide essentially all the available Mg. In the rat, approximately 15% of bone Mg (equivalent to 1.5 mmol/kg body weight) can be lost, whereas less than one tenth of that amount is available from skeletal muscle. In the human, up to 35% of bone Mg can be lost, but the mean loss in extant studies is 18% (equivalent to 1.2 mmol/kg body weight). In contrast to the rat, up to 40% of human skeletal-muscle Mg can be lost with an average loss of 15% (equivalent to 0.45 mmol/kg). In the human, the bone and skeletal-muscle Mg pools can provide an average of 1.7 mmol/kg body weight equivalent to 15% of total body Mg. Release of Mg from these stores appears to depend on the presence of hypomagnesemia which may also result in small, significant and potentially adverse Mg losses from certain vital organs such as the heart, kidney and brain. The liver and other organs appear not to lose Mg despite Mg deprivation although intracellular Mg shifts of importance cannot be ruled out. These data indicate that the body reserve to combat Mg depletion is not designed to protect the extracellular Mg pool and certain critical organs from Mg deficiency. A continuous optimal intake of Mg is needed for good nutrition and health.

Animals↗
PubMed1980

[The significance of magnesium in medicine. (II) Disturbances of magnesium metabolism and their treatment (author's transl)].

Magnesium (Mg) deficiency is common in diseases of the digestive tract and alcoholism, in diuretic therapy, hypocalcemia and as a congenital disturbance of absorption. The symptoms are particularly related to the heart and nervous system, but are not characteristic. Excess of Mg is observed in advanced renal failure. Compensation of the Mg deficiency partly explains the success of Mg in the treatment of cardiovascular, digestive and neuropsychiatric diseases. Parenteral feeding must contain adequate Mg. Important fields of application of Mg are the treatment of peptic ulcer and its use as a laxative.

Humans↗
PubMed1996

Oral physiological magnesium supplementation for 6 weeks with 1 g/d magnesium oxide does not affect increased Lp(a) levels in hypercholesterolaemic subjects.

Twenty hyperlipidaemic patients on a cholesterol-poor diet were selected on the basis of a raised lipoprotein (a) (Lp(a); apo (a) > 300 U/litre) and treated with 1000 mg MgO per day during 6 weeks. Serum magnesium slightly increased compared to pretreatment levels (P < 0.001). Serum apo(a) concentrations (mean +/- S.D.) were not affected: pretreatment level 963 +/- 552 U/litre; during treatment 999 +/- 536 U/litre; and after washout 995 +/- 524 U/litre. Serum cholesterol increased slightly during MgO treatment because of an increase in LDL-cholesterol (10 per cent) and returned to pretreatment levels after a washout period.

Administration, Oral↗
PubMed1990

Beneficial effect of magnesium on the isolated perfused rat heart during reperfusion after ischaemia: comparison between pre-ischaemic and post-ischaemic administration of magnesium.

The effect of high concentration of magnesium on both mechanical dysfunction and metabolic damage after ischaemia-reperfusion was studied in isolated rat hearts. The heart was perfused by the Langendorff's technique at a constant flow (10 ml/min) with modified Krebs-Henseleit solution and driven at 300 beats/min. The heart was made ischaemic by reducing the flow to 0 ml/min for 25 min, and then reperfused at the constant flow for 15 min. MgSO4 was added to the perfusate for 5 min before the onset of ischaemia, or after the end of ischaemia (after the onset of reperfusion). Ischaemia-reperfusion produced both mechanical dysfunction (as evidenced by an increase in the left ventricular end diastolic pressure and a decrease in the left ventricular developed pressure) and metabolic damage [as evidenced by a decrease in the myocardial adenosine triphosphate (ATP)]. When 15 mmol/l MgSO4 was given before ischaemia, there was no appreciable recovery of mechanical function, whereas when given after ischaemia (during reperfusion), there was a marked recovery of mechanical function. Lower concentrations (10 or 5 mmol/l) of MgSO4 given after ischaemia recovered the mechanical function concentration-dependently. The beneficial effect of 15 mmol/l MgSO4 was minimized by the coexistence of 4.5 mmol/l CaCl2 in the reperfusion solution. The decrease in the myocardial level of ATP induced by ischaemia-reperfusion was attenuated by 15 mmol/l MgSO4 given in the reperfusion solution. These results suggest that high Mg2+ is effective in attenuating both functional and metabolic damage of the post-ischaemic heart, provided it is given after ischaemia.

Adenosine Triphosphate↗
PubMed1997

Protective effect of magnesium supplementation on experimental 3-methyl cholanthrene-induced fibrosarcoma and changes in tissue magnesium distribution during carcinogenesis in rats.

In this study, we wanted to examine the effect of magnesium (Mg2+) supplementation on the experimental 3-methyl cholanthrene (3-MC)-induced fibrosarcoma and alterations in (Mg2+) distribution in several tissues of the rats, during carcinogenesis. It was determined that serum and tissue (Mg2+) levels of the rats in (Mg2+)-supplemented diet group were higher than those of the rats in the (Mg2+)-nonsupplemented and control groups. The mean time of fibrosarcoma development for (Mg2+)-supplemented group was longer than (Mg2+)-nonsupplemented group (p < 0.05). Symptoms of hypermagnesemia were not observed in any of the rats. These results suggests that dietary (Mg2+) supplementation may have a partial anti-carcinogenic effect on experimental 3-MC-induced fibrosarcoma by prolongation of the latent period of carcinogenesis.

Animals↗
PubMed1999

Total magnesium concentrations of perilymph, cerebrospinal fluid and blood in guinea pigs fed different magnesium-containing diets.

The total magnesium (Mg) concentrations of the perilymph (PL), cerebrospinal fluid (CSF), plasma and red blood cells (RBCs) of anesthetized guinea pigs separated into three groups and fed different Mg-containing diets were determined by atomic absorption spectrometry. Due consideration was given to the significant sources of error connected with the sampling procedure, particularly contamination of PL with CSF. The Mg levels of the individuals fluids differed significantly (P < 0.05/0.01) within each group. In the normal Mg group, the mean values of the PL, CSF and plasma were 0.66, 0.81 and 0.97 mmol/l, respectively, and 7.83 mmol/kg dry weight for RBCs. The analytical data were found to depend on the Mg content of the animals' diet, but to a different degree in the individual specimens (plasma > PL > CSF). A correlation was found to exist between all specimens tested (P < 0.05/0.01), except for CSF and RBCs, with the closest relation being that between plasma and PL. These findings suggest that the perilymphatic Mg equilibrates with the Mg level of plasma rather than with that of CSF. This is the first report showing Mg data of PL, CSF, plasma and RBCs obtained from the same subject, and the dependency on the Mg content of the animals' diet.

Animal Feed↗
PubMed2004

Physiological characterisation of magnesium deficiency in sugar beet: acclimation to low magnesium differentially affects photosystems I and II.

Magnesium deficiency in plants is a widespread problem, affecting productivity and quality in agriculture, yet at a physiological level it has been poorly studied in crop plants. Here, a physiological characterization of Mg deficiency in Beta vulgaris L., an important crop model, is presented. The impact of Mg deficiency on plant growth, mineral profile and photosynthetic activity was studied. The aerial biomass of plants decreased after 24 days of hydroponic culture in Mg-free nutrient solution, whereas the root biomass was unaffected. Analysis of mineral profiles revealed that Mg decreased more rapidly in roots than in shoots and that shoot Mg content could fall to 3 mg g(-1) DW without chlorosis development and with no effect on photosynthetic parameters. Sucrose accumulated in most recently expanded leaves before any loss in photosynthetic activity. During the development of Mg deficiency, the two photosystems showed sharply contrasting responses. Data were consistent with a down-regulation of PSII through a loss of antenna, and of PSI primarily through a loss of reaction centres. In each case, the net result was a decrease in the overall rate of linear electron transport, preventing an excess of reductant being produced during conditions under which sucrose export away from mature leaf was restricted.

Adaptation, Physiological↗
PubMed1992

Can the magnesium content of mononuclear blood cells be altered by oral magnesium supplementation?

A randomized, double-blind, placebo-controlled trial was performed on a rigorously defined group of normal subjects to see if magnesium (Mg) supplementation could affect serum Mg levels or Mg content of mononuclear blood cells. Forty-nine subjects were randomized to either placebo, tablets containing 90% United States recommended daily allowance (USRDA) of Mg, or tablets containing 180% USRDA of Mg. We were unable to demonstrate a statistically significant increase in Mg content of mononuclear blood cells.

Adult↗
PubMed1996

Reference interval for whole blood ionized magnesium in a healthy population and the stability of ionized magnesium under varied laboratory conditions.

OBJECTIVE: To establish a reference interval for ionized magnesium (iMg), to evaluate the stability of whole blood iMg under varied laboratory storage conditions, and to study the correlation between total and iMg in healthy volunteers and in an intensive care unit (ICU) population. METHODS: Blood specimens were collected anaerobically from 125 healthy volunteers and 200 ICU patients into tubes containing lithium heparin, transported to the laboratory on ice, stored at 4 degrees C and analyzed within 2 h on a NOVA 8 Electrolyte Analyzer. Additional specimens were stored under different conditions before analysis to assess the stability of iMg. RESULTS: In healthy volunteers, the mean whole blood iMg level was 0.52 mmol/L with a range of 0.44 to 0.59 mmol/L. The iMg/total serum Mg ratio was at 0.60 (0.50-0.69). Regression analysis of iMg vs total Mg produced a correlation coefficient (r) of 0.48 (p < 0.0001). Ionized Mg levels were comparable between males and females (0.52 +/- 0.04 vs 0.51 +/- 0.03, p = 0.38). In the ICU group, a wider range of iMg results was observed (0.35-0.78 mmol/L) and the correlation between iMg and total Mg was r = 0.71 (p < 0.0001). Storage of whole blood specimens in uncapped tubes at room temperature resulted in a small, but significant, decrease in iMg over a 6-h period. Little change was seen in capped tubes stored either at room temperature or at 4 degrees C. over 6 h, or at 4 degrees C. over 5 days. CONCLUSIONS: Using the NOVA 8 Electrolyte Analyzer, we established a reference interval for whole blood iMg in a healthy Canadian population. The correlation between ionized Mg and total Mg was weak, but statistically significant. Ionized Mg levels in lithium heparin tubes were stable over 5 days when specimens were stored at 4 degrees C, suggesting that specimens may be stored at least overnight prior to processing.

Adult↗
PubMed1996

Relationship between skeletal muscle intracellular ionized magnesium and measurements of blood magnesium.

The current laboratory approach to assessing magnesium status is based on determining the concentration of total Mg ((Mg)) in serum or plasma. This strategy is problematic in that the amount of Mg in blood is less than 1% of total body Mg and does not accurately reflect (Mg) in other tissues. Furthermore, the (Mg) of blood does not distinguish biologically active, ionized Mg from the bound fraction. The goal of this study was to determine intracellular ionized Mg ((Mg++)i) of skeletal muscle in vivo and to compare results with the (Mg) of blood constituents. (Mg++)i was determined in resting skeletal muscle by using phosphorus 31 magnetic resonance (31P-MR) spectroscopy. (Mg) was measured in serum (S(Mg)), serum ultrafiltrate (UF(Mg)), mononuclear blood cells (MBC(Mg)), and red blood cells (RBC(Mg)) by using atomic absorption spectroscopy or a colorimetric assay. In a sample of 60 healthy adult subjects, skeletal muscle (Mg++)i = 557 +/- 97 mumol/L (mean +/- SD); S(Mg) = 0.78 +/- 0.09 mmol/L; UF(Mg) = 0.60 +/- 0.12 mmol/L; MBC(Mg) = 13.8 +/- 2.3 mmol/L; and, RBC(Mg) = 1.92 +/- 0.33 mmol/L. A significant negative correlation was found between (Mg++)i and S(Mg) (r = -0.43, p < 0.05). S(Mg) was significantly lower (p < 0.05) and (Mg++)i significantly higher (p < 0.05) in women than in men, but neither was related to age. These findings provide new insight into the relationship between blood Mg measures and (Mg++)i of the largest soft tissue mass of the human body.

Adult↗
PubMed2002

Intracellular magnesium and magnesium buffering.

The development of new techniques for measuring intracellular free Mg2+ during the 1980s has provided investigators with the tools needed to produce new insights into the regulation of cellular magnesium. Within the limits of this technology, it appears that all mammalian cells maintain free cytosolic Mg2+ levels within the fairly narrow range of 0.25-1 mM. While transport mechanisms and sequestration within cellular organelles will contribute to this regulation, it is binding of Mg2+ to an as yet poorly defined system of buffers that is largely responsible for determining the set point of this regulation. The lack of an adequately Mg2+-selective ionophore remains an impediment to progress in this area.

Animals↗
PubMed2004

High intake of magnesium in relation to the ruminal transmural potential difference and magnesium absorption in wethers.

High potassium (K) intakes are known to decrease magnesium (Mg) absorption in ruminants by increasing the transmural potential difference (PDt, serosal side = positive). High Mg intakes are known to increase the amount of Mg absorbed, which may be explained by increasing the ruminal Mg concentration, but an effect on the PDt cannot be excluded. The objective of this study was to determine whether or not Mg intake affects the PDt. In a 3 x 3 Latin square design, six ruminally fistulated wethers were fed a low-Mg, low-K ration (3.88 g Mg/kg dry matter (DM); 30.7 g K/kg DM), a high-Mg, low K-ration (16.79 g Mg/kg DM; 30.7 g K/kg DM), and a low-Mg ration high-K (3.88 g Mg/kg DM or 62.1 g K/kg DM). When compared with the low-Mg, low-K ration, the high-Mg, low-K ration raised the absolute apparent Mg absorption (g/day) by 421% and the low-Mg, high-K ration decreased it by 20%. The intake of extra K produced a significant increase in the PDt. The intake of extra Mg did not change the PDt across the rumen wall but produced a significant increase of the ruminal Mg concentrations. On the basis of the individual values for three rations, the mean post feeding ruminal Mg concentrations were found to be unrelated to the PDt (Pearson's r = -0.329, p = 0.183, n = 18). Thus, it is concluded that the observed increase in Mg absorption after a high Mg intake can be explained by an increase in the ruminal Mg concentration rather than by a change in PDt.

Absorption↗
PubMed1990

Effect of intravenous epinephrine on serum magnesium and free intracellular red blood cell magnesium concentrations measured by nuclear magnetic resonance.

Hypomagnesemia is a common clinical finding in hospitalized patients and can cause hypocalcemia, cardiac arrhythmias, muscular weakness, and hypokalemia. Hypomagnesemia usually implies cellular magnesium (Mg) depletion, but stress and some clinical conditions which raise serum catecholamine concentrations may lower serum Mg (sMg) concentrations. To help investigate the mechanism and degree of the effect of catecholamines on sMg concentration, we gave intravenous epinephrine (0.1 microgram/kg/min) to 12 normal volunteers for 2 hours. The sMg concentration fell from 1.86 +/- 0.04 mg/dl to 1.63 +/- 0.05 mg/dl (mean +/- SEM, p less than 0.01). Pre-infusion intracellular free Mg (Mg++) in red blood cells (RBC) as measured by nuclear magnetic resonance spectrophotometry (NMR) was 171 +/- 7.6 microM and did not differ significantly from post-infusion RBC Mg++, 186 +/- 12.6 microM. Total blood mononuclear cell Mg content and urine Mg excretion also did not change. These data suggest that epinephrine has a small but significant effect on the lowering of sMg concentrations. Endogenous catecholamine release during stress or acute illness may therefore contribute to the hypomagnesemia seen in acutely ill patients. Our data also suggest that hypomagnesemia seen under conditions of acute stress may not always imply depleted tissue Mg stores. As no absolute change in cellular Mg or in urinary Mg excretion was demonstrated, acute intracellular shifts of Mg into blood cells and/or urinary Mg losses may not account for the hypomagnesemia. The prevalence and clinical consequences of stress hypomagnesemia require further investigation.

Adolescent↗