cholecalciferol and Magnesium-Deficiency

Topics: Cholecalciferol; Diagnosis, Differential; DNA-Binding Proteins; High Mobility Group Proteins; Humans; Hypoparathyroidism; Magnesium Deficiency; Mutation; Nuclear Proteins; Parathyroid Hormone; Prognosis; SOXB1 Transcription Factors; Transcription Factors

Topics: Alcoholism; Calcium; Cholecalciferol; Humans; Hypocalcemia; Magnesium; Magnesium Deficiency; Phosphorus Acids

The effect of a moderate magnesium (Mg) deficiency on coronary arteries of 61 swine, fed various levels of vitamin D3, was studied by light and electron microscopy. The effect of subnormal Mg intake on vitamin D3-induced intimal lesions of the arteries showed a trend towards increased damage. The degree of cell degeneration and intimal thickening, which was induced by high vitamin D intakes, was as great in swine whose diet was low in Mg and moderately high in vitamin D as it was in those on twice as much vitamin D. Also, the degree of arterial calcification was intensified by inadequate Mg intake at the two higher vitamin D intakes. Present findings indicate that suboptimal dietary Mg, in combination with an excess of vitamin D, has an additive effect in the initiation of ultrastructural changes in the coronary arteries. Extension of the study is indicated to ascertain the extent to which further reduction of Mg intake can potentiate vitamin-D-induced coronary lesions.

Topics: Animals; Arteries; Cholecalciferol; Coronary Vessels; Food, Formulated; Magnesium Deficiency; Male; Swine

Magnesium ion is of great importance in physiology by its intervention in 300 enzymatic systems, its role in membrane structure and its function in neuromuscular excitability. The skeleton is the first pool of magnesium in the body. Intestinal absorption, renal metabolism, bone accretion and resorption of magnesium are very similar to those of calcium. Magnesium metabolism is accurately controlled, in particular by parathyroid hormone, 25 - dihydroxy vitamin D3, calcitonin, catecholamine and estrogens. The main regulation mechanisms of magnesium metabolism are located in the kidney which is the principal excretory organ.

Topics: Calcitonin; Calcium; Cholecalciferol; Estrogens; Female; Humans; Kidney; Magnesium; Magnesium Deficiency; Male; Parathyroid Hormone; Potassium; Pregnancy

Topics: Alcoholism; Animals; Cholecalciferol; Choline Deficiency; Ethanol; Fatty Liver; Glutamates; Humans; Hyperlipidemias; Hypoglycemia; Intestinal Absorption; Iron; Ketones; Liver Cirrhosis; Magnesium Deficiency; Mitosis; Nutritional Physiological Phenomena; Rats; Thiamine; Thiamine Deficiency; Uric Acid; Vitamin B 6 Deficiency; Zinc

Vitamin D is synthesized in the skin or supplied. Cholecalciferol is hydroxylated in the liver to 25(OH) vitamin D [25D]. 25D is further hydroxylated in the kidney to 1,25(OH) vitamin D [1,25D]. Catabolism occurs by further hydroxylation. Magnesium is a cofactor of all involved hydroxylases.. To investigate the association between renal function and serum magnesium levels, and the biologically active hormone 1,25D.. Anonymised serum values of 25D, 1,25D, magnesium and creatinine measured in an outpatient cohort over 2 years were analysed.. Renal function and magnesium level did not influence 25D values (r = - 0.144 and 0.030, respectively). Mean serum 1,25D values decreased from 106.5 ± 44.3 pmol/l in individuals with normal renal function to 51.7 ± 18.9 pmol/l in those with severe renal insufficiency (p < 0.01). A weak positive correlation was observed between 1,25D and eGFR (r = 0.317), and between 1,25D and serum magnesium (r = 0.217).. Impaired renal function and low magnesium serum levels are slightly associated with low 1,25D concentrations. Measuring 25D, but not 1,25D, may overestimate the patient's vitamin D status. In patients with renal insufficiency adequate magnesium supply should be ensured.

Topics: Cholecalciferol; Humans; Magnesium; Magnesium Deficiency; Renal Insufficiency; Vitamin D; Vitamin D Deficiency; Vitamins

The rate of total secretion of saliva was measured over a 3-h period, under steady state conditions, in conscious sheep. The rates of secretion of magnesium and calcium in saliva represented 25-30% of the magnesium and calcium in the extracellular fluid. Since the large stores of intracellular magnesium are not readily mobilizable, the only readily available reserve of magnesium to maintain magnesium homeostasis is a little in bone. Thus, if magnesium ions from food and saliva are not adequately reabsorbed in the fore-stomachs, their loss could contribute significantly to the failure of homeostasis noted in acute ruminant hypomagnesaemia. Studies of the salivary clearance of 28 Mg showed a delay of 5-13 h in the time course of the salivary specific activity of 28 Mg, relative to that in plasma. This delay is indicative of transcellular interchange between magnesium ions in the central compartment, represented by the extracellular fluid, and an outer compartment which includes the salivary epithelial cells. Prolonged hypercalcaemia, caused by injections of 1 alpha (OH) cholecalciferol, was accompanied by a significant increase in the secretion rate of calcium in saliva but the secretion rate of magnesium was unchanged.

Topics: Animals; Calcium; Cholecalciferol; Homeostasis; Magnesium; Magnesium Deficiency; Magnesium Sulfate; Saliva; Sheep; Sheep Diseases

In contrast to man, the rat exhibits hypercalcemia during the course of magnesium depletion. To investigate the role of the vitamin D (D) endocrine system in the induction of hypercalcemia, circulating D metabolites, the binding properties of the duodenal 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] receptor (VDR), and 45Ca transport studies were undertaken in magnesium-replete rats or after 10 days of magnesium depletion in animals presenting the following D status: D depletion and hypo- or normocalcemia (achieved by oral calcium supplementation), D3 or 1,25-(OH)2D3 repletion. Magnesium depletion did not influence serum calcium in hypo- or normocalcemic D depleted rats, but increased serum calcium in animals receiving D3 (P less than 0.002) or 1,25-(OH)2D3 (P less than 0.0001), suggesting that the D3 endocrine system is necessary to mediate the rise in extracellular calcium and that dietary calcium alone is not sufficient to significantly increase extracellular calcium in the hypomagnesemic rat. The data also show that 25-hydroxyvitamin D formation was not perturbed, but circulating 1,25-(OH)2D3 concentrations were reduced by 10 days of magnesium depletion (P less than 0.0001) even in animals infused with 1,25-(OH)2D3, suggesting increased clearance of the hormone. The kinetic data of the duodenal VDR revealed maximum binding sites ranging from 1018-1500 fmol/mg DNA and Kd ranging from 0.17-0.38 nM, with no significant between-group difference in magnesium-sufficient animals. Ten days of magnesium depletion did not significantly influence VDR affinity in any of the groups, but significantly increased receptor number in hypocalcemic D-depleted rats from 1190 +/- 154 to 2748 +/- 430 fmol/mg DNA (P less than 0.004). Calcium transport studies in D-replete animals indicate that intestinal calcium transport is influenced by the progressive depletion in magnesium, with time-related increases coinciding with the in vivo increase in circulating ionized calcium (day 6 of magnesium depletion). However, despite persistent elevated serum ionized calcium, calcium transport declined only to predepletion levels on days 8 and 10 of magnesium depletion. To investigate the influence of the D3 endocrine system on 45Ca absorption, D-depleted rats sufficient or depleted in magnesium were injected with 1,25-(OH)2D3, either acutely (to reveal its membrane effects) or 16 and 5 h before death (to reveal its genomic effect). The data reveal a reduced response in magnesium-depleted rats

Topics: Analysis of Variance; Animals; Calcifediol; Calcitriol; Calcium; Cholecalciferol; Duodenum; Female; Magnesium; Magnesium Deficiency; Male; Rats; Rats, Inbred Strains; Receptors, Calcitriol; Receptors, Steroid; Vitamin D Deficiency

Topics: Adenosine Triphosphatases; Amino Acids; Child, Preschool; Cholecalciferol; Fanconi Syndrome; Humans; Hypophosphatemia, Familial; Infant; Kidney Diseases; Kidney Tubules; Magnesium; Magnesium Deficiency; Male; Phosphorus; Potassium