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Results for “Magnesium Deficiency”

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PubMed2001

In vivo and in vitro effects of magnesium deficiency on hepatic haptoglobin mRNA levels.

We previously showed that haptoglobin (Hp) was increased in the plasma of dietary magnesium (Mg)-deficient rats. The present study was performed to examine the effects of dietary Mg-deficiency and Mg2+ deficit in culture medium on Hp mRNA levels in liver and isolated hepatocytes, respectively. The Hp mRNA level in the liver increased significantly from day 10 to day 30 in rats on a Mg-deficient diet (Mg; 0.001 per cent). In the cultured hepatocytes, lowering the Mg2+ level in the culture medium from 0.92 mM to 0.46 mM did not affect the Hp mRNA level of hepatocytes. When IL-1beta or IL-6 was added to the culture medium, the Hp mRNA level increased much more in the hepatocytes cultured in low Mg2+ medium (Mg2+; 0.46 mM) than in those cultured in the control Mg2+ medium (Mg2+; 0.92 mM). These results suggest that the increase in plasma Hp level during dietary Mg deficiency depends on the increase in Hp mRNA level in the liver, and that this increase in mRNA is not only directly correlated with a low Mg level in plasma, but also indirectly correlated with cytokines.

Animals↗
PubMed2001

Magnesium deficiency in patients with recent myocardial infarction and provoked coronary artery spasm.

This study sought to clarify the relationship between magnesium (Mg) deficiency and coronary artery spasm provoked by pharmacologic agents in patients with a recent acute myocardial infarction (AMI). Twenty-three consecutive patients suffering from AMI were investigated with a Mg retention test (Mg: 0.1 mmol/kg for 4 h) in both the acute phase (within I week (3+/-2 days) of onset) and the subacute phase (3-4 weeks (24+/-6 days) of the onset). Early coronary arteriography was performed in all patients. Coronary stenosis in the infarct-related artery was less than 90% in all patients in the subacute phase. The spasm provocation test was performed in the subacute phase and coronary spasm was defined as transient subtotal or total occlusion in association with angina or electrocardiographic ST-segment deviation. Coronary artery spasm was provoked in only 13 of the 23 patients. Compared with the control subjects (12 patients without coronary artery disease or coronary spasm), the 24-h Mg retention was significantly higher in patients with AMI (acute phase: 78+/-27%, subacute phase: 66+/-32%, vs control: 48+/-12%, p<0.05). In the subacute phase, the 24-h Mg retention decreased in patients without coronary spasm (43+/-26%), but a high level of Mg retention was still observed in patients with coronary spasm (84+/-25%). There was no difference in the serum concentrations of Mg, calcium and phosphorus between the 2 groups on both phases. In conclusion, both Mg deficiency and provoked coronary artery spasm were noted in more than half of the Japanese patients with a recent AMI, suggesting a close association between Mg deficiency and AMI.

Aged↗
PubMed2002

Magnesium deficiency during pregnancy in rats increases systolic blood pressure and plasma nitrite.

We investigated the effect of moderate dietary magnesium (Mg) deficiency, pregnancy, and concurrent L-arginine ingestion on systolic blood pressure (BP), nitric oxide production, serum Mg, and intrauterine growth restriction. Female rats, fed Mg deficient or sufficient diets from weaning, were divided into three groups: (1) nonpregnant, (2) pregnant, and (3) pregnant + 1% L-arginine in the drinking water. The systolic BP, plasma nitrite, serum Mg, and pup weights were determined. Data were analyzed using general linear model analysis of variance. In the pregnant rats, the Mg-deficient group had a significantly higher systolic BP (P =.0275) and plasma nitrite (P =.0244) compared to the Mg-sufficient group. L-Arginine ingestion significantly lowered systolic BP (P <.0001), and increased pup weight (P <.0067). Among the deficient groups, serum Mg was significantly lower (P =.0010) in pregnant rats without L-arginine, but was similar to the nonpregnant state in pregnant Mg-deficient after ingesting L-arginine. Moderate Mg deficiency, during the stress of pregnancy, adversely affected BP, nitric oxide production, and serum Mg. Supplemental L-arginine prevented these negative effects, possibly through a feedback loop by increasing nitric oxide syntheses, which increases cyclic guanosine monophosphate, which then increases free Mg and decreases free calcium. These ionic changes can act to decrease BP and modulate nitric oxide synthesis.

Animals↗
PubMed1974

Magnesium deficiency: a possible cause of thiamine refractoriness in Wernicke-Korsakoff encephalopathy.

The determination of blood transketolase before and serially after thiamine administration, and the response of clinical symptomatology after thiamine are reported in two normomagnesaemic patients and one hypomagnesaemic patient with acute Wernicke-Korsakoff encephalopathy. The response of the depressed blood transketolase and the clinical symptoms was retarded in the hypomagnesaemic patient. Correction of hypomagnesaemia was accompanied by the recovery of blood transketolase activity and total clearing of the ophthalmoplegia in this patient, suggesting that hypomagnesaemia may be a cause of the occasional thiamine refractoriness of these patients.

Alcohol Amnestic Disorder↗
PubMed1974

Effects of magnesium deficiency on the photosynthesis and respiration of leaves of sugar beet.

The effects of Mg deficiency on the photosynthesis and respiration of sugar beets (Beta vulgaris L. cv. F58-554H1) were studied by withholding Mg from the culture solution and by following changes in CO(2) and water vapor exchange of attached leaves. Leaf blade Mg concentration decreased from about 1200 to less than 200 meq kg(-1) dry matter without change in the rate of photosynthetic CO(2) uptake per unit leaf area, while from 200 to 50 meq kg(-1) the rate decreased to one-third. Rates of photorespiratory evolution of CO(2) into CO(2)-free air responded to Mg like those of photosynthetic CO(2) uptake, the rates decreasing to one-half, below 200 meq kg(-1). Respiratory CO(2) evolution in the dark increased almost 2-fold in low Mg leaves. Magnesium deficiency had less effect on leaf (mainly stomatal) diffusion resistance (r(1)) than on mesophyll resistance (r(m)); in Mg-deficient plants r(m) increased from 2.9 to 7.1 sec cm(-1), whereas r(1) became significantly greater than the control value only in the most severe instances of Mg deficiency.

Journal Article↗
PubMed1992

Beneficial effects of a calcium antagonist, nifedipine, on death and cardiovascular calcinosis induced by dietary magnesium deficiency in adult mice.

The effects of nifedipine on the survival rate and the cardiovascular calcinosis were investigated in dietary magnesium (Mg)-deficient mice. Male mice aged 8 to 10 weeks were fed with a diet which was either normal (0.07%) or deficient (0.007%) in Mg for 30 d. Nifedipine was added to the Mg-deficient diet for 30 d in a concentration of 1000 ppm. About 65% of Mg-deficient mice died within 30 d. In contrast, all the nifedipine-treated mice survived for 30 d. Mg-deficient mice showed hypomagnesaemia and hypocalcaemia which were not influenced by nifedipine treatment. Aortic and cardiac calcium contents increased in Mg-deficient mice, and these increments were normalized by nifedipine treatment. These results suggest that the life-saving effect of nifedipine in Mg-deficient mice might relate, at least in part, to the prevention of a deleterious increase in Ca in cardiovascular tissues.

Animals↗
PubMed2006

Dietary calcium supplementation suppresses bone formation in magnesium-deficient rats.

The purpose of this study was to clarify the effects of dietary calcium (Ca) supplementation on bone metabolism of magnesium (Mg)-deficient rats. Male Wistar rats were randomized by weight into three groups, and fed a control diet (control group), a Mg-deficient diet (Mg- group) or a Mg-deficient diet having twice the control Ca concentrations (Mg-2Ca group) for 14 days. Trabecular bone volume was significantly lower in the Mg- and Mg-2Ca groups than in the control group. Trabecular number was also significantly lower in the Mg- and Mg-2Ca groups than in the control group. Mineralizing bone surface, mineral apposition rate (MAR), and surface referent bone formation rate (BFR/BS) were significantly lower in the Mg- and Mg-2Ca groups than in the control group. Furthermore, MAR and BFR/BS were significantly lower in the Mg-2Ca group than in the Mg- group. These results suggest that dietary Ca supplementation suppresses bone formation in Mg-deficient rats.

Analysis of Variance↗
PubMed1989

Enhanced contractile response to noradrenaline and calcium influx in thoracic aorta isolated from dietary magnesium deficient rats.

Dependency on extracellular calcium influx in contractile response to noradrenaline has been investigated in the thoracic aorta isolated from dietary magnesium (Mg) deficient rats. Adult male Wistar rats were fed with a Mg deficient diet (0.001% Mg) for 30 days, together with control groups (0.07% Mg). The contractile response to noradrenaline in the thoracic aortas from Mg deficient rats was significantly greater than that in the controls. However, there were no significant differences between control and Mg deficient rats in the contractile response to high potassium. The rate of 45Ca uptake induced by noradrenaline was greater in Mg deficient rat aortas than in the controls, but that induced by high potassium showed no significant differences between control and Mg deficient rats. Calcium entry blockers (verapamil and nifedipine) caused a concentration-dependent depression of the noradrenaline-induced contraction. The aortas from Mg deficient rats were more sensitive to these drugs than were those from the controls. These results suggest that the noradrenaline-induced contraction depends much more on extracellular calcium influx in Mg deficient rats than in the controls.

Animals↗