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Results for “Magnesium Deficiency”

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PubMed1996

Bone histomorphometry of ovariectomized or orchiectomized rats fed a moderately magnesium-deficient fructose diet and treated with exogenous oestrogen or testosterone.

To investigate the effects of sex hormones on bone histomorphometry, and bone density (BMD), 10 week old ovariectomized (OVX), orchiectomized (ORX), and sham-operated (SHAM) rats fed a moderately magnesium-deficient fructose diet were studied. One third of the OVX and ORX rats were injected with beta-oestradiol-3-benzoate; another third, testosterone cypionate; and the remaining SHAM rats, vehicle only. After 14 weeks, a 24 h urine sample was collected for measurements of calcium, phosphorus and cyclic AMP (cAMP). Blood was collected for determination of calcium, phosphorus, and parathyroid hormone (PTH). Femurs and tibias were removed and weighed. Femurs were used to measure bone areas, mineral contents (BMC), and BMD. Tibias were used for bone histomorphometry (that is, trabecular numbers, thicknesses, % areas and separations). Oestrogen treatment increased serum and urine calcium significantly in both OVX and ORX rats, whereas testosterone decreased serum and urine calcium significantly. Oestrogen decreased urinary cAMP and PTH in both OVX and ORX rats, whereas testosterone treatment increased them significantly. Oestrogen treatment increased BMD, trabecular numbers, thicknesses, and % areas, and decreased bone separations in both OVX and ORX rats. In contrast, testosterone did not increase these bone indices in either OVX or ORX rats; rather, it increased bone separations by decreasing bone strength. Testosterone treatment improved trabecular histomorphometry slightly in OVX rats. The results of the present study are concordant with our previous findings that exogenous oestrogen treatment can prevent osteoporosis in either OVX or ORX rats, whereas exogenous testosterone cannot.

Anabolic Agents↗
PubMed1994

Cholesterol oxides in plasma and lipoproteins of magnesium-deficient rabbits and effects of their lipoproteins on endothelial barrier function.

The cholesterol oxide (ChO) levels in the plasma and low density lipoproteins (LDL and VLDL) in four groups of rabbits fed for seven weeks either normal (NC) or high cholesterol (HC) with low or normal magnesium (Mg) diets were determined and compared with the NC group fed a standard rabbit diet. The plasma from the NC group contained low levels of different cholesterol oxides. These cholesterol oxides were significantly elevated in the plasma of rabbits fed a HC-normal magnesium or a HC-low magnesium diet. In the NC-low Mg group, 7 alpha-hydroxycholesterol, 7 beta-hydroxycholesterol and 7-ketocholesterol were elevated while the other cholesterol oxides remained within the normal range of the NC group. When the cholesterol oxides were assayed in the LDL and VLDL fractions as micrograms/mg protein, the fractions obtained from the groups fed NC-low Mg, HC-normal Mg or HC-low Mg diets showed higher levels of cholesterol oxides than the fractions obtained from the NC group. When LDL and VLDL fractions from the different groups were incubated at equal protein concentration with confluent endothelial cell monolayers, transendothelial albumin transfer was significantly increased by the lipoproteins from the experimental groups as compared to the control group. These results suggest that elevation of cholesterol oxides in magnesium deficiency or hypercholesterolaemia may be related to their atherogenic effects through decreasing the endothelial barrier function which could enhance the deposition of cholesterol rich lipoproteins into the arterial wall.

Animal Feed↗
PubMed1992

Refractory potassium repletion. A consequence of magnesium deficiency.

Experimental and clinical observations support the view that uncorrected magnesium (Mg) deficiency impairs repletion of cellular potassium (K). This is consistent with the observed close association between K and Mg depletion. Concomitant Mg deficiency in K-depleted patients ranges from 38% to 42%. Refractory K repletion due to unrecognized concurrent Mg deficiency can be clinically perplexing. Refractory K repletion as a consequence of Mg deficiency may be operative in patients with congestive failure, digitalis toxicity, cisplatin therapy, and in patients receiving potent loop diuretics. Therefore, we recommend that: (1) serum Mg be routinely assessed in any patients in whom serum electrolytes are necessary for clinical management and (2) until serum Mg is routinely performed consideration should be given to treating hypokalemic patients with both Mg as well as K to avoid the problem of refractory K repletion due to coexisting Mg deficiency.

Electrolytes↗
PubMed2000

Magnesium efficacy in magnesium deficient and nondeficient patients with rapid ventricular response atrial fibrillation.

We assessed the effect of magnesium sulphate (MgSO4) on lowering the rate in ventricular atrial fibrillation (AF), and evaluated the effect of this therapy in magnesium (Mg) deficient and nondeficient patients. This experimental clinical study was performed on 34 patients with rapid AF (ventricular rate [VR] > 120/minute) presenting to the emergency department of a tertiary care university hospital. Patients with systolic blood pressure < or = 100 mmHg, Hb level < or = 11.8, saO2 of < or = 96%, BUN > or = 40 or creatine > or = 1.8 were excluded (n = 15). Nineteen patients were given an initial 2 g MgSO4 bolus i.v. and a 1 g/hour continuous infusion over 6 hours. To evaluate the presence of Mg deficiency, urine was collected from the onset of treatment and continued for the next 24 hours, and the excretion rate of administered Mg was calculated. Ventricular rates were obtained at baseline, after MgSO4 bolus, and every 15 minutes for the first hour. The decrease in the VR was statistically significant at 15, 30 and 60 minutes after Mg therapy (p = 0.0025, p < 0.001, p > 0.001). There was no difference in the response to Mg therapy between Mg deficient and nondeficient patients at 15, 30 or 60 minutes after therapy (p = 0.41, p = 0.28, p = 0.08). It is concluded that i.v. MgSO4 has a statistically significant but clinically limited effect on VR and this effect did not differ between patients with and without Mg deficiency.

Adult↗
PubMed1979

The differential effect of magnesium deficiency on isoenzymes of alkaline phosphatase (EC 3.1.3.1) in rat tissues.

1. Alkaline phosphatase (EC 3.1.3.1) from many rat tissues was separated into two or three bands by electrophoresis on polyacrylamide gel. Ten of the bands had different electrophoretic mobilities, but some were present in more than one tissue. 2. Bands from the corresponding tissues of magnesium-deficient and control rats were qualitatively similar, but there were quantitative differences in the distribution of enzyme activity between them. 3. Mg deficiency had differential effects on the absolute activity of individual bands, but two main types of response were observed. There was an increase in the activity of the first bands from liver and kidney, the second band from femur and both bands from spleen, whereas the first band from femur, the first and second bands from intestinal mucosa and the second bands of serum, liver and kidney all decreased in activity during the deficiency. 4. The change in total alkaline phosphatase activity of a tissue during Mg deficiency depended on the ratio between the enzyme components within it.

Alkaline Phosphatase↗
PubMed1991

Magnesium deficiency affects plasma lipoprotein composition in rats.

Weanling rats were pair-fed for 8 d with control and Mg-deficient diets containing 960 and 30 mg of Mg/kg, respectively. The marked reduction in plasma Mg levels indicated that the rats fed the Mg-deficient diet were indeed deficient. In the Mg-deficient rats the percent composition of triglycerides in VLDL, LDL and HDL was elevated and that of protein was reduced. Although the proportion of cholesterol was reduced in LDL and HDL, that of phospholipid was decreased only in HDL. Magnesium deficiency induced a decrease in the percent composition of apolipoprotein (apo) E and a relative increase in the apo C for VLDL. In HDL from Mg-deficient rats, the proportion of apo AI was higher than normal, apo AIV was lower than normal and apo E was virtually absent. The percent composition of oleic and linoleic acids was increased but that of stearic and arachidonic acids was depressed in both VLDL and HDL derived from Mg-deficient rats compared with pair-fed controls. Whether these alterations in lipoprotein profile contribute to hyperlipoproteinemia or are the results of the metabolic changes that produce hyperlipoproteinemia remain to be determined.

Animals↗
PubMed2000

Effect of magnesium deficiency on enterocyte Ca, Fe, Cu, Zn, Mn and Se content.

In previous studies based on indirect procedures, we reported that Mg deficit increased the bioavailability of a number of elements such as calcium, zinc, iron, copper, manganese and decreased selenium absorption. The present study was designed to verify these findings by direct methods. We investigated the effect of dietary magnesium deficiency on enterocyte Ca, Fe, Zn, Cu, Mn and Se concentrations. Male Wistar rats were fed a Mg-deficient diet (129 mg Mg/kg food) for 70 days. Whole enterocytes from the upper jejunum were isolated and Ca, Fe, Zn, Cu, Mn and Se were determined. The results were compared with findings in a control group that was pair-fed with an identical diet except that it covered this species's nutritional requirements for Mg (480 mg Mg/kg food). The Mg-deficient diet significantly increased enterocyte content of Ca, Fe, Zn, Cu and Mn; however, we found no significant changes in the Se content of these cells. These data support the results obtained by indirect methods.

Animals↗
PubMed1987

Hypocalcemic crisis in alcoholic fatty liver: transient hypoparathyroidism due to magnesium deficiency.

Hypocalcemic crisis developed in a patient with acute alcoholic fatty liver. In addition to jaundice and marked hepatomegaly, the patient presented with hypocalcemic crisis associated with hypomagnesemia, low plasma 1,25(OH)2-vitamin D and undetectable plasma parathyroid hormone (PTH) concentration. Subsequent computerized tomographic scan and liver biopsy showed the presence of severe fatty liver. With the improvement of liver function, the serum calcium level increased, and was accompanied by normalization of plasma PTH, serum magnesium, and plasma 1,25(OH)2-vitamin D levels. Serial ethylenediaminetetraacetic acid infusion tests demonstrated the reversal of the impaired PTH secretion. Thus, hypocalcemic crisis in this patient appeared to result from transient hypoparathyroidism induced by magnesium deficiency.

Acute Disease↗
PubMed2002

Changes in N-acetyl-beta-D-glucosaminidase activity in the urine and urinary albumin excretion in magnesium deficient rats.

To discover the details of the effects of magnesium (Mg) deficiency on kidney function, the course of changes in N-acetyl-beta-D-glucosaminidase (NAG) activity in the urine and in urinary albumin excretion were examined in rats fed a Mg-deficient diet. NAG activity in the urine and urinary albumin excretion in rats fed the Mg-deficient diet significantly increased from 7 d until the end of the feeding period. We suggest that Mg-deficient diet rapidly induces kidney function insufficiency.

Acetylglucosaminidase↗
PubMed2006

Urinary excretion of an intravenous 26Mg dose as an indicator of marginal magnesium deficiency in adults.

BACKGROUND: Measurement of magnesium (Mg) status is problematic because tissue Mg deficiency can be present without low serum Mg concentrations. OBJECTIVE: To evaluate a modified version of the Mg retention test using stable isotopes for the assessment of Mg status in general, and the detection of marginal Mg deficiency in particular. DESIGN: A modified version of the Mg retention test using a small dose of (26)Mg was evaluated for assessment of Mg status in 22 healthy subjects. Muscle Mg concentration was used as reference for Mg status. A muscle biopsy was taken from the lateral portion of the quadriceps muscle from each subject. After 2 to 4 weeks, 11 mg of (26)Mg (as MgCl(2) in 14 ml water) were injected i.v. over a period of 10 min and all urine was collected for the following 24 h. Excretion of the isotopic label was expressed as percentage of the administered dose excreted in urine within 24 h. RESULTS: Mean +/- s.d. Mg concentration in muscle was 3.85 +/- 0.17 mmol/100 g fat-free dried solids. Mean +/- s.d. excretion of the injected dose within 24 h was 7.9 +/- 2.1%. No correlation was found between muscle Mg concentration and excretion of the isotopic label (r (2 ) = 0.061, P = 0.27). CONCLUSIONS: In this study, urinary excretion of an intravenous Mg tracer was not influenced by muscle Mg concentration and its usefulness for the detection of marginal Mg deficiency could therefore not be demonstrated. SPONSORSHIP: Swiss Foundation for Nutrition Research and Swiss Federal Institute of Technology, Zurich, Switzerland.

Adult↗
PubMedDate not supplied

Ultrastructure of the optic nerve in magnesium-deficient rats.

PURPOSE: The ultrastructure of the optic nerves in magnesium (Mg)-deficient rats was studied to elucidate the function of Mg. METHODS: After delivery, mother Wistar Kyoto rats were fed a low-Mg diet containing 0.1 mg Mg/100 g diet with all other nutrients and distilled and deionized water. Infant rats were suckled by their mothers for 21 days and then fed the same Mg-deficient diet. Control mother rats were fed commercial rat pellets containing 24 mg Mg/100 g diet and all other nutrients. The optic nerves were examined by electron microscopy at 6 weeks of age. RESULTS: In the Mg-deficient rats, serum Mg levels were significantly lower and calcium levels higher than in the control rats. Ultrastructural findings were: significantly fewer myelinated axons and significantly thinner myelin sheaths in the Mg-deficient rats than in the control and pair-fed controls, and more numerous unmyelinated axons. There were multifocal areas of destruction and necrosis in the optic nerve of Mg-deficient rats. CONCLUSIONS: This study suggests that the optic nerve needs Mg for the development and maintenance of its cell structure.

Animals↗
PubMed1997

Changes in bioavailability and tissue distribution of selenium caused by magnesium deficiency in rats.

OBJECTIVE: We investigated the effect of dietary magnesium (Mg) deficiency on the bioavailability and tissue distribution of selenium (Se). METHODS: Wistar rats were fed an Mg-deficient diet for 70 days (D). Selenium content in plasma, whole blood, skeletal muscle, heart, kidney and femoral bone was determined after 7, 35, 49 and 70 days on a Mg-deficient diet. RESULTS: The Mg-deficient diet significantly decreased Se absorption from week 7 until the end of the experimental period; this effect was accompanied by a significant decrease in Se balance. We found a direct linear correlation between Se absorption and retention (balance) (pair-fed controls r = 0.842, p < 0.001; Mg-deficient rats r = 0.959, p < 0.001), and between Se absorbed and plasma Se concentration (controls r = 0.527, p < 0.02; Mg-deficient rats r = 0.704, p < 0.001). In general there were no significant correlations between urinary Se and any other parameter. Tissue analyses showed that after 7 days, Mg deficiency reduced erythrocyte Se and significantly increased plasma and kidney Se. Heart Se was significantly increased only at the end of the study. We found no significant changes in skeletal muscle or bone Se at any time during the experimental period. CONCLUSION: Chronic Mg deficiency decreases Se absorption and retention and erythrocyte concentrations of this mineral, and increases Se in plasma, kidney and heart. Under our experimental conditions, absorption appears to play an important role in the regulation of the tissue distribution of Se.

Animals↗