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PubMed1994

Increase of streptozocin toxicity by magnesium deficiency in the diabetic rat model.

To study interactions between magnesium (Mg) and diabetes mellitus, female SD-rats weighing ca. 230 g were rendered Mg-deficient by offering a diet providing only 20% of the rat's requirement. After 14 days the animals were injected 75 mg streptozocin (STZ) per kg body weight intraperitoneally. Placebo-treated controls received the same diet, however their drinking-water was enriched with 20 mmol/l Mg as the magnesium-L-aspartate hydrochloride. Mg deficiency remarkably increased STZ-induced lethality from 3.8% to 61.1% on day 35. Pronounced hyperglycemia and necrosis of pancreatic beta cells also suggest an increased effect of STZ on the pancreas during Mg deficiency. The underlying mechanisms are discussed. Food consumption was decreased in Mg-deficient animals and steeply increased 7 days following STZ treatment. Similarly consumption of drinking-water also increased. Since diabetic rats lost body weight, relative and absolute Mg intake via food or drinking-water increased. In this way further Mg depletion of diabetic rats was prevented.

Animals↗
PubMed1995

Magnesium deficiency in critically ill patients.

A study was performed to assess the value of estimation of intracellular magnesium in peripheral blood cells (red and mononuclear blood cells) in critically ill patients as an index of tissue magnesium content. A magnesium loading test was used to diagnose magnesium depletion in 16 critically ill patients. Patients were divided into magnesium depleted and non-depleted groups according to their response to the loading test. Pre-infusion plasma and intracellular (blood cell) magnesium levels were measured. There were no significant difference between the magnesium depleted (mean plasma magnesium 0.81 mmol.l-1, red blood cell magnesium 2.34 mmol.l-1, mononuclear blood cell magnesium 25.16 mmol.kg-1 dry weight) and non-depleted groups (mean plasma magnesium 0.90 mmol.l-1, red blood cell magnesium 2.18 mmol.l-1, mononuclear blood cell magnesium 18.1 mmol.kg-1 dry weight). We conclude that the diagnosis of magnesium depletion cannot be excluded in the face of normal plasma, red blood cell or mononuclear blood cell concentrations of magnesium.

Critical Illness↗
PubMed1992

Effect of chronic maternal dietary magnesium deficiency on placental calcium transport.

Metabolisms of calcium (Ca) and magnesium (Mg) are closely interrelated in the intestine, bone, and kidney. Interaction of Ca and Mg at the placental level, however, is not well defined. The occurrence of decreased bone mineral content and hypocalcemia in infants of hypomagnesemic mothers led us to test the hypothesis that chronic dietary maternal Mg deficiency decreases placental Ca transport. On day 10 of gestation, 20 Sprague-Dawley rats were randomized to a Mg-deficient diet (3.3 mg/day, n = 10) or to a control diet (70 mg/day, n = 10). On day 20 of gestation (term = 22 days), intact placentas were perfused in situ through the umbilical artery and perfusate was collected through the umbilical vein. Calcium 45 (45Ca) and chromium 51-EDTA (51Cr-EDTA) (a diffusional marker for placental membrane integrity) were injected to the dam and steady state maternofetal clearance (Kmf45Ca, microliter/min/g placenta) of both isotopes were calculated. There was no difference in the clearance of 45Ca and 51Cr in both groups (55 +/- 10 vs 57 +/- 16 and 3.2 +/- 0.4 vs 3.6 +/- 0.4, respectively, mean +/- SEM). We conclude that, in the rat, placental Ca transfer is unaffected by chronic maternal dietary Mg deficiency. We speculate that Ca and Mg cross the placenta by independent mechanisms.

Animals↗