Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Magnesium Deficiency”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed1984

Histamine content and histidine decarboxylase activity in the spleen of the magnesium-deficient rat: comparison with the skin and peritoneal mast cells.

In young rats, some effects of magnesium (Mg) depletion in the diet on histamine content and histidine decarboxylase (HDC) activity in spleen were studied in comparison with those in the skin and peritoneal mast cells. In the case of the young rats fed a Mg-deficient diet (0.001% Mg), the splenic histamine contents increased to levels about 1.3, 2.8 and 23 times as high as those in the rats fed a control diet (0.07% Mg) on the 4th, 6th and 8th day, respectively; histamine contents in the peritoneal mast cells also increased to about 1.2 and 1.8 times the control levels on the 6th and 8th day, respectively; no change was observed in histamine contents in the skin during 8 days of Mg depletion. HDC activities in the spleen of Mg-deficient rats on the 4th, 6th and 8th day increased to levels about 5.5, 15.5 and 35 times as high as the respective control values; the activities in the skin increased to about 37, 7 and 10 times the control values on the 4th, 6th and 8th day, respectively; while in the peritoneal mast cells, the activities increased to about 1.2 and 2.2 times the control values on the 6th and 8th day, respectively. On the 8th day of the Mg deficiency, some studies were made on the effects of histamine releasers on histamine contents in the spleen and peritoneal mast cells. Compound 48/80 (0.5 microgram/ml) or polymyxin B (5 micrograms/ml) induced a release of histamine from the peritoneal mast cells, but not from the spleen cells isolated from the Mg-deficient rat in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Magnesium deficiency differentially affects the retina and visual cortex of intact rats.

To determine the influence of magnesium (Mg) on the visual system, electroretinograms (ERG) and visual evoked potentials (VEP) were recorded under dark-(DA) and light-adapted (LA) conditions in intact rats. Weanling rats were fed either a Mg-deficient (Mg-D) or a control diet for 17 d before the tests, and ERG, VEP and immunohistopathological analyses of retinae and cortices were made. In the Mg-D rats, ear congestion, hair loss and loss of body weight were observed, and serum Mg concentration was approximately 25% of that in the control rats (P < 0.01). The amplitudes of the DA a-wave and the second positive peak of the oscillatory potentials (OP2) of the ERG, and the negative component of the VEP (N1) in Mg-D rats were significantly greater than those of control rats. However, the amplitudes of the DA b-wave, LA 2 Hz b-wave, the 20 Hz flicker responses and the implicit times of all response components did not differ between the two groups. The immunohistopathologic results also were not altered in the Mg-D rats. We suggest that the functional abnormalities induced by Mg deficiency may depend not only on the hyperactivity of the N-methyl-D-aspartate (NMDA) receptor, but also on the behavior of the Ca(2+) and Mg(2+) ions in the intact eye.

Animals↗
PubMed2004

A functional biological marker is needed for diagnosing magnesium deficiency.

Functional biological markers or biomarkers are now available for many nutrients which are used as nutritional status markers. Most sources of these biomarkers are products or precursors of enzymatic processes that can be measured in serum and plasma. At this time measurements of total or ionized magnesium (Mg) in serum, plasma, cellular components, urine or Mg retention from a load test are performed, but they may not always reflect Mg nutritional status. Biomarkers for Mg are needed which would reflect changes in biochemical processes where Mg is involved. Biomarkers for Mg need to be identified and evaluated in both animals and humans, with a determination of possible factors that may affect the reaction and biomarker concentrations. Some possible biomarkers for Mg include the following: Na/K ATPase, thromboxane B2, C-reactive protein, and endothelin-1. Other possible biomarkers for Mg need to be identified.

Adenosine Triphosphatases↗
PubMed1991

Skeletal buffer function and symptomatic magnesium deficiency.

A major factor relating to the oversight of neurological dysfunction and seizures caused by magnesium (Mg++) depletion, involves the buffer functions of the skeletal system orchestrated primarily by the parathyroid. A Mg++ depleted subject may appear relatively asymptomatic until a short period after homeostatic responses go into effect. The results can be devastating if not recognized promptly and treated appropriately. This series of events can best be demonstrated in veterinary medicine but we propose that analogous syndromes occur in clinical medicine. Evidence is presented to support the hypothesis that in subjects with parathyroid hyperactivity and Mg++ deficiency, the stimulus of a rise in serum ionic calcium (Ca++), and the resultant inhibition of parathyroid hormone (PTH) secretion, trigger the transfer of Ca++, Mg++ and other ions from the extracellular space into the exchangeable bone compartment. More importantly, there is a transfer of Mg++ ions from the cerebrospinal fluid into the blood and ultimately into the bone compartment. If the gradient is large and the stimulus adequate, neurological signs and symptoms may be induced. The degree of Ca++ and Mg++ depletion of the peripheral bone and the amount and duration of Ca++ ion increase largely determine the duration and severity of symptoms. The symptom complex is facilitated by sympathetic stimulation. An analogous situation may exist with sodium (Na+).

Animals↗
PubMed2005

Immunolocalization of RANKL is increased and OPG decreased during dietary magnesium deficiency in the rat.

BACKGROUND: Epidemiological studies have linked low dietary magnesium (Mg) to low bone mineral density and osteoporosis. Mg deficiency in animal models has demonstrated a reduction in bone mass and increase in skeletal fragility. One major mechanism appears to be an increase in osteoclast number and bone resorption. The final pathway of osteoclastogenesis involves three constituents of a cytokine system: receptor activator of nuclear factor kB ligand (RANKL); its receptor, receptor activator of nuclear factor kB (RANK); and its soluble decoy receptor, osteoprotegerin (OPG). The relative presence of RANKL and OPG dictates osteoclastogenesis. The objective of this study was to assess the presence of RANKL and OPG in rats on a low Mg diet. METHODS: RANKL and OPG were assessed by immunocytochemistry staining in the tibia for up to 6 months in control rats on regular Mg intake (0.5 g/kg) and experimental rats on reduction of dietary Mg (.04%, 25% and 50% of this Nutrient Requirement). RESULTS: At all dietary Mg intakes, alteration in the presence of immunocytochemical staining of RANKL and OPG was observed. In general, OPG was decreased and RANKL increased, reflecting an alteration in the RANKL/OPG ratio toward increased osteoclastogenesis. CONCLUSION: We have, for the first time demonstrated that a reduction in dietary Mg in the rat alters the presence of RANKL and OPG and may explain the increase in osteoclast number and decrease in bone mass in this animal model. As some of these dietary intake reductions in terms of the RDA are present in a large segment of or population, Mg deficiency may be another risk factor for osteoporosis.

Journal Article↗
PubMed1989

Dietary fructose as compared to glucose and starch increases the calcium content of kidney of magnesium-deficient rats.

The effects of feeding diets containing fructose, glucose or starch with or without added magnesium (Mg) on tissue levels of calcium (Ca) in weanling rats were investigated. Rats were fed their respective diet for 4 wk and then fasted overnight. After decapitation, blood was immediately collected, and liver, kidney and heart were removed to determine their Mg and Ca content. Relative kidney and liver weights were greatest in the rats fed the fructose diet. Hypomagnesemia was observed in all animals fed a Mg-deficient diet regardless of carbohydrate source (1.71 vs. 2.27 mg Mg/dl plasma for Mg-deficient vs. Mg-adequate groups, respectively). Among Mg-deficient groups, starch-fed rats had the highest level of plasma Mg, while fructose-fed rats had the highest level of kidney Mg. Although plasma and liver Ca levels were not significantly different among the groups, Ca content of the kidney and heart was greatest in animals fed a Mg-deficient diet with fructose. This was especially evident in the Ca content of the kidney, which was 8- to 9-fold greater than that of all other experimental groups. The results of the present study demonstrate the presence of a synergistic interaction between fructose and Mg deficiency that increases Ca levels in certain soft tissues, especially the kidney.

Animals↗
PubMed1983

Effects of dietary magnesium deficiency on thallium-20 1 kinetics and distribution in rat myocardium: concise communication.

Kinetics and distribution of TI-201 were studied in myocardium of rats with chronic dietary induced Mg deficiency. Rats were fed the Mg-deficient diet for 30 days and were then injected intravenously with 0.2 mCi of TI-201. Comparable control animals were fed a standard laboratory diet. One-half hour after injection, rats were killed and a segment of myocardium was washed with nonradioactive Krebs solution in a special chamber. Radioactivity in the tissue was recorded continuously for 1 hr. A three-compartment model (extracellular, main intracellular, and subcellular) was found to describe adequately the kinetics of TI-201. In myocardium of Mg-deficient animals, significant changes in values of transport rate constants and compartment sizes for TI-201 indicated a moderate decrease in extracellular compartment and a threefold enlargement in subcellular compartment (presumably mitochondrial) at the expense of the main intracellular compartment, which underwent a marked reduction. Bulk TI-201 uptake in myocardium of Mg-deficient rats was unchanged. The findings are interpreted as being consistent with mitochondrial alterations reported in Mg-deficient animals. Clinical implications are discussed.

Animals↗