Magnesium Turnover Research Articles

Renal Magnesium Handling Is Not Subject to Developmental Programming

Developmental programming of hypertension, induced by maternal protein restriction, is associated with enhanced urinary excretion of sodium and calcium in the rat. Although calcium and magnesium are reabsorbed via different pathways, renal calcium excretion often parallels magnesium output. Accordingly, the aim of the current study was to assess magnesium handling in rats exposed to a low-protein (LP) diet in utero. Wistar rats were fed a control (18%) or LP (9%) diet throughout pregnancy; offspring were weaned onto standard rat chow and studied at 4 weeks of age. Renal clearance measurements were made in both volume expanded and euvolaemic anaesthetised rats; 24-hour magnesium turnover was also assessed in conscious animals. Plasma and total body magnesium content were measured. Total (U_MgV) and fractional excretion (FE_Mg) of magnesium did not differ between control and LP rats under any of the experimental conditions. Neither plasma nor total body magnesium content differed between control and LP rats. Thus the hypercalciuria of LP rats is not mirrored by an increase in renal magnesium excretion. These data suggest that renal magnesium handling is not affected by developmental programming.

Exchangeable magnesium pool masses in healthy women: effects of magnesium supplementation

Studying magnesium pools in the body with use of stable isotopes may be helpful for evaluating magnesium status. Data on the evaluation of magnesium pools in humans are scarce. We undertook this study to evaluate the effects of a magnesium supplementation program on the size of the exchangeable body pools of magnesium and on classic indexes of magnesium status in healthy women with normal magnesium status. Ten healthy women participated in a kinetic study with magnesium stable isotopes before and after 8 wk of magnesium supplementation. Each woman received 3 supplements containing 5.08 mmol (122 mg) elemental Mg/d (366 mg/d). Before and at the end of the supplementation period, each woman received an intravenous injection of 1.67 mmol (40 mg) (25)Mg, and the plasma magnesium disappearance curve was followed for the next 7 d. Two methods were used to analyze the exchangeable pools of magnesium: 1) formal multicompartmental modeling and 2) a simplified estimation of the total mass of the rapidly exchangeable magnesium pool (EMgP). In these healthy women, exchangeable magnesium pools represented 11-12% of total body magnesium on the basis of multicompartmental analysis. The simplified estimation of EMgP overestimated the size of the exchangeable magnesium pools by approximately 45-50%. Eight weeks of magnesium supplementation did not significantly modify the size of the exchangeable magnesium pools, whereas urinary magnesium excretion was significantly higher after 8 wk of supplementation. Women with no clinical evidence of magnesium deficiency may not respond to short-term supplementation with increases in the mass of the exchangeable magnesium body pool or in magnesium turnover rates.

Effects of magnesium deficiency on magnesium and calcium content in bone and cartilage in developing rats in correlation to chondrotoxicity.

Quinolone-induced arthropathy has been described in juvenile rats between 3 and 6 weeks of age, but not in adult rats. The mechanism of this chondrotoxic effect is probably related to the Mg2+-chelating properties of the drugs, since identical cartilage lesions were observed in magnesium-deficient juvenile rats without quinolone treatment. However, the reasons for the phase-specificity of the effect are unknown. In the present study, we fed a magnesium-deficient diet to Wistar rats at different postnatal developmental stages. Cartilage lesions were only observed in magnesium-deficient rats between 3 and 5 weeks of age, but not in rats receiving the magnesium-deficient diet during weeks 5 to 8, weeks 8 to 11, or months 15 to 16. The formation of cartilage lesions was not related to the magnesium concentration in plasma, since magnesium concentrations in plasma were similarly reduced in rats with and without cartilage lesions. However, chondrotoxicity correlated with magnesium content in articular cartilage. In articular cartilage (articular and epiphyseal cartilage in immature rats) and bone, magnesium content was more reduced in rats receiving the magnesium-deficient diet between 3 and 5 weeks of age as compared with rats receiving the magnesium-deficient diet during weeks 8 to 11 postnatally. It was not possible to reduce the magnesium content in bone tissue of 15-month-old Wistar rats, which suggests a lower magnesium turnover in aged rats. Magnesium content in epiphyseal cartilage of 2-week-old rats (total femoral head) was 41.9 +/- 16.9 mmol/kg dry weight. The magnesium content in joint hyaline cartilage was significantly lower in 4-week-old rats (19.5 +/- 3.6 mmol/kg dry weight) and increased subsequently again to 48.5 +/- 9.2 mmol/kg dry weight (mean +/- SD; n = 8 to 16). Increase of the magnesium content in femoral bone between weeks 4 and 6 postnatally was less pronounced (139 +/- 10 and 175 +/- 15 mmol/kg dry weight, respectively). Taken together, these data show that in 4-week-old rats, magnesium concentration in joint hyaline cartilage is significantly lower than at other times during postnatal development. Only at this developmental stage can cartilage lesions be induced by feeding rats a magnesium-deficient diet. This period correlates well with the sensitive phase of immature rats toward the chondrotoxic action of quinolones.

Feasibility of measuring organ magnesium turnover in vivo by continuous feeding of a stable isotope

The feasibility of measuring organ endogenous magnesium (Mg en) turnover in vivo by continuous feeding of a single stable isotope of Mg was demonstrated in this investigation. Adult CD-1 mice were fed a Mg deficient diet and deionized water with (+Mg) or without (−Mg) added 24Mg (290 μg/mL) for 16 days. The change in organ 25Mg content over time was then accurately determined by in vitro isotope dilution with 26Mg as spike. Organ endogenous Mg content was then calculated as 25Mg en/ 0.1028 and exogenous Mg (Mg ex) content from the expression Mg ex = Mg total - Mg en . All soft tissues examined in the +Mg group showed significant turnover of Mg en and accumulation of Mg ex. The rate at which this occurred was organ specific. Apparent half-lives for Mg en turnover were 3.83, 4.13, 5.87, and 8.77 days for liver, heart, brain, and skeletal muscle, respectively. Mg restriction resulted in a dramatic decrease in the rate of Mg en turnover with apparent half-lives ranging from 60.3 to 146 days. Brain showed the smallest decrease in Mg en turnover with Mg restriction, and was the only tissue observed to lose a significant amount of total Mg.

Calcium, phosphorus and magnesium turnover.

The body content of calcium, phosphorus and magnesium is important, not only from the structural or supporting aspect, but also from the aspect of cellular function. Membrane integrity, nervous tissue conduction, neuromuscular excitability, muscle contraction, hormone secretion, intermediary metabolism and synthesis, to mention but a few activities, are all influenced by these elements. The normal body content and turnover of calcium, phosphorus and magnesium are outlined, together with a brief description of their physiological roles, emphasizing intracellular functions rather than their predominance within the skeleton. Regulatory mechanisms, particularly for calcium, involving vitamin D and its metabolites, parathormone, and possibly calcitonin, are discussed within the context of maintaining normal body content and turnover. Homeostatic mechanisms maintaining plasma concentrations in health and disease, as far as they have been identified, are also outlined. Lastly, disorders of calcium, phosphorus and magnesium turnover are considered from the aspect of altered plasma concentrations of these substances. Throughout emphasis is given to common problems and their practical management. Metabolic bone disease and uncommon disorders of bone and bone mineral are not discussed specifically.

Magnesium transport in humans with hypomagnesemia.

ABSTRACT The kinetics of radiomagnesium exchange were measured in 9 human subjects with moderate hypomagnesemia and 1 normomagnesemic patient with demonstrated magnesium deficiency. Eight of the 10 patients were alcoholics with associated hepatic dysfunction and disturbances in the plasma concentrations of other electrolytes as well as hypomagnesemia. Three normomagnesemic patients with alcoholism and hepatic cirrhosis were also studied. A digital computer program utilizing a parallel 3-compartment open model of magnesium exchange was employed for quantitation of the primary data. At the time of study, 2–9 weeks after hospital admission, normal kinetics of magnesium exchange were found in almost all subjects. The data also indicated that conventionally calculated apparent exchangeable body pools of magnesium show a borderline correlation with computer derived values for the exchangeability of magnesium and are therefore not reliable parameters of magnesium turnover. Despite moderate hypomagnesemia and/or ...

Role of magnesium metabolism and the effects of fluoride therapy in Paget's disease of bone.

ABSTRACT Magnesium metabolism has been examined in 5 patients with active Paget's disease of bone with the use of 28MgCl2 and a multicompartmental-type analysis to describe the isotopic and metabolic data. Serial studies were also performed in one patient before, immediately following 1 yr of treatment with sodium fluoride, and 1 yr after sodium fluoride had been discontinued when both clinical and chemical evidence of recurrent disease were apparent. The results support the view that prolonged administration of large doses of sodium fluoride are beneficial in Paget's disease. The data also define abnormal magnesium metabolism in this disorder as reflected in a significant decrease in exchangeable magnesium and abnormal increments in magnesium turnover. The chronic administration of sodium fluoride to one patient with Paget's disease resulted in a suppression of the pathologically accelerated magnesium turnover and a reversion of exchangeable magnesium values toward normal. This investigation provides fur...

TISSUE DISTRIBUTION OF ELECTROLYTES, CA47, AND MG28 IN ACUTE HYPERCALCEMIA.

The in vivo effects of acute hypercalcemia on plasma and tissue distribution of electrolytes, radiocalcium, and radiomagnesium were studied in acutely renal-ligated dogs. Hypercalcemia abruptly increased plasma potassium and phosphorus concentrations but had no significant effect on plasma concentrations of other electrolytes. Skeletal muscle and myocardial sodium decreased 15%, skeletal muscle chloride decreased 22%, and pancreatic and aortic potassium increased 12%. Tissue phosphorus concentrations were unchanged. Total cellular calcium increased 40–70% in liver, myocardium, nerve, and aorta, was suggestively increased in skeletal muscle, and was unchanged in pancreas, brain, and bone. Exchangeable cellular calcium increased 35–75% in liver, skeletal muscle, myocardium, nerve, and aorta and was unchanged in pancreas and brain. Bone exchangeable calcium increased 260%. Exchangeable cellular magnesium of skeletal muscle and pancreas decreased 28% but total cellular magnesium concentrations were unaltered. The changes noted in individual tissues were reflected by 50% increases in exchanged able body and over-all tissue calcium pools and in unchanged exchangeable body and over-all tissue magnesium pools. No significant changes in fractional rates of calcium and magnesium turnover occurred. These data indicate that hypercalcemia causes 1) cellular accumulation of calcium by many but not all tissues, 2) inhibition of magnesium uptake by certain cells, and 3) changes in tissue sodium and potassium distribution which are compatible with known in vitro inhibitory effects of calcium on cellular electrolyte transport.

Placental transfer and fetal tissue uptake of Mg28 in the rabbit.

SummaryMg28 was injected intravenously into 11 pregnant rabbits between 28 and 30 days of gestation. Fetuses and placentas were removed at intervals ranging from 7 minutes to 26 hours. Maternal tissue uptake of Mg28 resembled that previously found in nonpregnant young adult rabbits, except that uptake in bone and muscle was slower. Concentration of Mg28 in the placenta rapidly rose above the maternal plasma level. Specific activity of magnesium in all fetal tissues studied reached a fairly constant value by 26 hours. Magnesium turnover in tissues of the fetus in utero, especially in bone and muscle, is considerably more rapid than that in the respective tissues of the mother.Mg28 was supplied by Brookhaven Laboratory on allccation from U. S. Atomic Energy Comm.

The Kinetics of Magnesium Distribution Within the Sheep

SUMMARY Carrier-free Mg28 was injected intravenously into sheep and the corrected plasma specific activity/time curves obtained. Each could be subdivided into 3 components by the use of a graphical logarithmic analysis. From them, the magnesium turnover time was calculated and estimates made of the total labile and total exchangeable body magnesium. By the use of the isotope dilution method the endogenous faecal excretion of magnesium was calculated and the true daily magnesium excretion obtained. From the corrected plasma Mg28 decay curve an estimate of the total true daily excretion of magnesium was derived. This was in good agreement with that observed. With the aid of these excretion data calculations were made of the time intervals likely to elapse before clinical hypomagnesaemia became manifest under varying conditions of magnesium absorption and endogenous faecal magnesium excretion. It is suggested that clinical hypomagnesaemia may result from a combination of reduced magnesium absorption and increased excretion of endogenous faecal magnesium.