Effect Of Magnesium Depletion Research Articles

Effects of magnesium depletion on inflammation in chronic disease.

To update findings supporting the opinion that commonly occurring subclinical magnesium deficiency induced by a low dietary intake is a predisposing factor for chronic inflammatory stress that contributes to the incidence of chronic diseases such as cardiovascular disease and diabetes. Both deficient magnesium intakes (<250 mg/day) and serum magnesium concentrations (≤ 0.75 mmol/l) have been associated with elevated serum C-reactive protein concentration, a widely used indicator of inflammation. Achieving magnesium intakes or serum magnesium concentrations that indicate an adequate magnesium status generally attenuates elevated serum C-reactive protein to concentrations that are not indicative of chronic low-grade inflammation. Individuals that are obese or have chronic diseases for which low-grade inflammation is a risk factor are commonly found to be magnesium-deficient. Subclinical magnesium deficiency caused by low dietary intake often occurring in the population is a predisposing factor for chronic inflammatory stress that is conducive for chronic disease. Magnesium deficiency should be considered a nutrient of significant concern for health and well-being.

Tetany and rhabdomyolysis due to surreptitious furosemide--importance of magnesium supplementation.

Diuretics may induce hypokalemia, hypocalcemia and hypomagnesemia. While severe hypokalemia may cause muscle weakness, severe hypomagnesemia is associated with muscle spasms and tetany which cannot be corrected by potassium and calcium supplementation alone (1,2). Surreptitious diuretic ingestion has been described, mainly in women who are concerned that they are obese or edematous. Symptomatic hypokalemia has been reported in such patients (3-7) and in one case hypocalcemia was observed (8), but the effects of magnesium depletion were not noted in these patients.

Effects of magnesium depletion on myocardial high-energy phosphates and contractility

The effect of prolonged magnesium depletion on contractility, phosphorylating activity, and organic phosphates of spontaneously beating isolated rat atria was studied. Rats were fed a Mg-deficient diet for 8 weeks, during which serum Mg fell from 1.85 ± 0.02 to 0.52 ± 0.10 mg/dl. Atrial contractile activity was measured for 1 hr and at the end of this period tissue samples were taken for the determination of the phosphorylated intermediates. Mg depletion was associated with (a) reduced intracellular inorganic phosphorus and adenine nucleotides; (b) elevated creatine phosphate; (c) reduction in contractile force (CF) with no change in atrial beat rate (BR). There were no significant differences in the activities of creatine phosphokinase and adenylate kinase in control and Mg-depleted rat atrial homogenates determined in the presence of 5 m m MgCl 2. Addition of various concentrations of MgCl 2 to the medium resulted in an immediate reduction in both CF and BR of normal and Mg-depleted rat atria. Intraperitoneal administration of MgCl 2 to Mg-depleted rats resulted in complete recovery of CF of isolated atria. This improvement in CF occurred without changes in the levels of inorganic phosphate and adenine nucleotides. The reduced intracellular level of high-energy phosphate or inorganic phosphate cannot therefore be responsible for the impaired contractility seen in Mg-depleted heart muscle. On the other hand, the fact that the creatine phosphate levels were higher in magnesium depletion suggests that myofibrillar utilization of creatine phosphate is more impaired than production, analogous to phenomena seen in postanoxic recovery.

Effect of magnesium depletion on metabolism of 25-hydroxyvitamin D in rats.

Resistance to vitamin D in magnesium depletion has been observed in humans and in animal studies. Variable levels of 1,25-dihydroxyvitamin D [1,25(OH)2D] have been reported in patients with magnesium depletion, and studies of vitamin D metabolism in states of magnesium depletion have not yielded consistent results. We examined effects of magnesium deprivation on circulating 1,25(OH)2D levels before and after a loading dose of 25-hydroxyvitamin D3 [25(OH)D3], on in vivo conversion of small doses of radiolabeled 25(OH)D3 to 1,25(OH)2D3 in intact rats, and on in vitro 25-hydroxyvitamin D-1 alpha-hydroxylase (1 alpha-hydroxylase) activity in rat renal mitochondria. The effects of magnesium-free media on mitochondrial 1 alpha-hydroxylase activity was examined. Magnesium depletion did not affect in vivo conversion of 25(OH)D to 1,25(OH)2D. In vitro 1 alpha-hydroxylase activity was comparable in magnesium-replete and -deplete animals and was evident in the absence of added magnesium in incubation media. Our in vivo and in vitro studies are consistent with one another and demonstrate that in the rat conversion of 25(OH)D to 1,25(OH)2D is unimpaired in magnesium deficiency. Resistance to vitamin D in magnesium depletion is likely due to the impaired skeletal responsivity to 1,25(OH)2D, as demonstrated in earlier studies.

The Effect of Magnesium Depletion on Thyroid Function in Rats

The effects of dietary magnesium (Mg) depletion on thyroid function were studied in young male rats. The rats were fed a semipurified diet containing either 12 ppm Mg (deficient rats) or 662 ppm Mg (control rats) for 14 to 28 days. Results showed that the Mg-deficient rats had decreased body weight gain, lowered concentrations of plasma thyroxine (T4) and Mg, but increased weight of the thyroid gland when expressed in proportion to the body weight (milligrams/100 g). There was no difference in the accumulation (uptake) of 131I, 24 hours after Na131I injection, between the Mg-deficient and Mg-supplemented rats. The protein-bound 131I (PB131I) level and the ratio of PB131I to total 131I in plasma was significantly reduced in Mg-deficient rats. Serum thyroid-stimulating hormone (TSH) levels after thyrotropin-releasing hormone injection (TRH, 50 ng/100 g body weight) increased fivefold at 30 minutes, but declined to near the basal level at 2 hours in both groups. No consistent difference in TSH response was observed between the two treatments. Serum T4 response to TRH challenge was significantly reduced in Mg-deficient as compared to Mg-adequate rats at all time intervals. The reduction of T4 level could be due to an impaired T4 synthesis or release in Mg-deficient rats.

Adsorption isotherms of albumin and ferritin on Rhodesian chrysotile: Effects of magnesium depletion

Adsorption isotherms of bovine albumin and horse spleen ferritin on Rhodesian chrysotile were evaluated. At an equilibrium concentration of 0.2 μ m/liter both proteins reached saturation condition and 0.17 μ m/g of both proteins were adsorbed by fibers. Albumin showed a decreased affinity to chrysotile depleted by EDTA of 31% of its magnesium content, while specific adsorption of ferritin increased. The role of surface charges on fibers and proteins was discussed.

The Effect of Magnesium Depletion on the Electrocardiogram and Plasma Electrolytes in Liver Cirrhosis

The Effect of Magnesium Depletion on the Electrocardiogram and Plasma Electrolytes in Liver Cirrhosis

Hypocalcemia in magnesium-depleted dogs: Evidence for reduced responsiveness to parathyroid hormone and relative failure of parathyroid gland function

The effect of magnesium depletion on serum calcium and magnesium and on the response to the infusion of parathyroid extract (PTE) was evaluated in nine adult mongrel dogs during a control period, magnesium depletion, and following magnesium repletion. Magnesium depletion was associated with a fall in serum magnesium and calcium, and both returned to normal with magnesium repletion. There was a significant direct correlation between the serum concentration of calcium and magnesium in the magnesium-deficient state. During magnesium depletion, there were significant calcemic and phosphaturic responses to PTE, but these effects were reduced; the impaired responsiveness of the skeleton and the kidney to PTE returned to normal after magnesium repletion. Serum levels of immunoreactive parathyroid hormone, measured in two animals during the control and magnesium depletion state, remained stable during magnesium depletion, despite the hypocalcemia present. These results indicate that both impaired responsiveness of the skeleton to parathyroid hormone and reduced secretion of the hormone in response to hypocalcemia exist in dogs with magnesium depletion. Each of these factors probably contributes to a reduced level of serum calcium in magnesium depletion, and they may compound each other and hence aggravate the degree of hypocalcemia.

Effect of magnesium depletion on responsiveness to parathyroid hormone in parathyroidectomized rats.

Hypocalcemia and resistance to exogenous parathyroid hormone have been reported in several clinical states associated with magnesium deficiency. On the basis of such observations, it has been suggested that magnesium depletion per se may result in impaired responsiveness of the adenyl cyclase-adenosine 3',5'-monophosphate (3',5'-AMP) system. To test this hypothesis, 4 wk old male parathyroidectomized rats were maintained on normal or magnesium-deficient diets for 4 wk and their responses to parathyroid hormone compared. Serum magnesium and calcium fell progressively in the magnesium-deficient group. Despite clinical and biochemical evidence of severe magnesium deficiency in these animals, renal production and excretion of 3',5'-AMP in response to parathyroid hormone was normal both in vitro and in vivo. Additionally, administration of either dibutyryl 3',5'-AMP or parathyroid extract to fasting magnesium-depleted rats produced a normal increase in serum calcium. Parathyroid hormone infusion studies demonstrated normal renal and skeletal responsiveness as measured by urinary excretion of calcium, magnesium, phosphate, and hydroxyproline. These data show that the effect of parathyroid hormone on 3',5'-AMP formation and excretion, the responsiveness of skeletal tissue to 3',5'-AMP, and the renal and skeletal system responses to parathyroid hormone are not altered by pure magnesium deficiency in the parathyroidectomized rat.

Effect of magnesium depletion on renal function in the rat.

Abstract Magnesium depletion was induced in 30 female Holtzman rats by feeding them a diet containing only 1 mg. of magnesium per 100 Gm. Various parameters of renal tubular function were measured in these rats and in 30 pair-fed controls receiving the same diet with the addition of 40 mg. of magnesium per 100 Gm. The diet was adequate in potassium content. Polyuria developed in the test rats 14 to 18 days after the deficient diet was instituted. At this time the maximum urinary concentration following vasopressin and thirst had decreased by 33 per cent from the controls. At the second week of depletion, the test rats were able to excrete only 50 per cent as much titratable acid in response to an ammonium chloride load as the controls. A marked phosphoresis appeared in the magnesium-depleted animals as early as one week and increased to thirtyfold by the fourth week. Pronounced urinary conservation of magnesium occurred in the depleted animals within one week. Urinary calcium excretion also decreased. Plasma and muscle magnesium decreased significantly in the test animals, whereas potassium levels were not altered. It is concluded that magnesium deficiency induces significant functional impairment in the renal tubules of rats which closely resembles that of potassium depletion.