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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of high calcium intake on vitamin D metabolism were investigated. To the normal diet of 14 healthy men, 2 g calcium were added daily for 6-7 weeks. The mean serum concentration of 25-hydroxyvitamin D3 increased from 73 +/- 7 to 94 +/- 6 nmol l-1 (P less than 0.05, Student's unpaired t-test; P less than 0.01, paired t-test) in the subjects receiving calcium, whereas there was only a minimal increase, from 67 +/- 5 to 71 +/- 4 nmol l-1 in a control group on a normal diet. At the end of the study the difference between the test group and the controls was highly significant (P less than 0.005). The calcium loading caused a statistically significant depression of the serum levels of 1,25-dihydroxyvitamin D. The results obtained are in agreement with previous studies in rats and indicate that calcium intake is of some importance for the serum level of 25-hydroxyvitamin D3. The findings are discussed in relation to our previous finding that there is a relationship between high 25-hydroxyvitamin D3 levels and hypercalciuria in renal-stone formers.
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PMID:Effect of calcium intake on serum levels of 25-hydroxyvitamin D3. 313 Feb 59

Two experiments were carried out on 2-week-old chicks in which they were fed protein-deficient diets for varying lengths of time with or without calcium (Ca). All deficient diets depressed the rate of growth; this depression was more marked in chicks fed the protein-deficient diet for 21/2 days than in those fed the diet for 4 days. The circulating growth hormone level was high in all protein-deficient diets but low in the diet only deficient in calcium. The low Ca-induced-rise in renal vitamin D, 1-hydroxylase activity was reduced, and the plasma Ca level was particularly low, in chicks on the low protein/low Ca diet. The 24-hydroxylase activity was high on the low protein diets. It was concluded that adaptation to a low protein diet occurs over the first 4 days and that this may be associated with the high growth hormone level and also that adequate dietary protein is essential for maximal adaptation to dietary Ca deficiency.
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PMID:The effect of low levels of dietary protein and calcium on growth rate, growth hormone, and vitamin D metabolism in the chick. 326 3

Incubation of 25-hydroxyvitamin D3 with kidney cortex mitochondria from 1,25-dihydroxyvitamin D3-treated guinea pigs resulted in the formation of 23,25-dihydroxyvitamin D3 as the major product. The identity of the product was verified by g.c.-m.s. and quantification was performed by h.p.l.c. The rates of the reaction were in the range 1.0-1.8 pmol/min per mg of mitochondrial protein (at 37 degrees C), which were 5-10 times the rates of formation of 24,25-dihydroxyvitamin D3. In mitochondrial preparations from untreated guinea pigs, the rate of 23-hydroxylation was below detection limit (0.02 pmol/min per mg of mitochondrial protein). Fasting the animals for 24 h induced the 23-hydroxylase almost as efficiently as treatment with 1,25-dihydroxyvitamin D3, with a concomitant depression of the 1 alpha-hydroxylase. The 23-hydroxylase reaction required oxidizable substrate, was decreased by low O2 partial pressures and inhibited by CO or the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone. It was stimulated by the respiratory-chain inhibitors rotenone, antimycin A and KCN. These results indicate that the guinea-pig renal mitochondrial 23-hydroxylase is a cytochrome P-450 and that the reducing equivalents are primarily supplied by NADPH via the energy-dependent transhydrogenase.
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PMID:Assay and properties of 25-hydroxyvitamin D3 23-hydroxylase. Evidence that 23,25-dihydroxyvitamin D3 is a major metabolite in 1,25-dihydroxyvitamin D3-treated or fasted guinea pigs. 335 35

Sensorineural hearing loss has been frequently reported in patients with renal failure but its etiology has not yet been established. Disturbance of Ca metabolism is present in renal failure and seems to cause hearing loss. The purpose of the present study was to determine whether the disturbance of Ca metabolism has any effect on cochlear function. The cochlear potentials were measured in 19 rats fed with a vitamin D deficient diet. The pathological findings showed prolongation of N1 latency with unchanged N1 amplitude and pseudothreshold, depression of CM amplitude and elevation of the CM pseudothreshold. The latencies of narrow-band APs were prolonged in the entire cochlear partition. Ca2+ concentration in perilymph was 3.2 X 10(-4) M (n = 4) in vitamin D deficient rats and 7.4 X 10(-4) M (n = 4) in the controls. These findings were milder than those obtained in surgically induced renal failure. It was concluded that although vitamin D deficiency is one cause of hearing loss in renal failure, other major factors must be involved. The authors postulate that hearing loss in vitamin D deficiency is mainly attributable to the depression of the Ca2+ concentration in perilymph.
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PMID:The effect of vitamin D deficiency on the cochlear potentials and the perilymphatic ionized calcium concentration of rats. 347 52

Betamethasone (50 micrograms/kg body weight/day) given to young pigs reduced calcium absorption, growth and plasma vitamin D dependent calcium binding protein (CaBP) concentration. No changes occurred in plasma 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and intestinal CaBP concentrations. 1,25(OH)2D3 (0.1 microgram/kg body weight/day) given with betamethasone increased calcium absorption although growth and plasma CaBP concentrations remained low. Intestinal CaBP levels remained unchanged. Plasma CaBP concentrations were not consistently related to intestinal CaBP or calcium absorption in the presence of betamethasone. We conclude that betamethasone-induced depression of calcium absorption was not mediated by alterations in intestinal CaBP, but the mechanism remains obscure.
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PMID:The effects of betamethasone on plasma and intestinal calcium binding protein and on 25-hydroxyvitamin D3 metabolism in the pig. 375 94

Large white male turkey poults were fed diets with different levels of vitamins A and D to study the interaction of these vitamins with regard to skeletal development. Poults fed a basal diet deficient in both vitamins A and D developed severe lameness, growth depression, mortality and lesions consistent with rickets. Birds fed a diet containing the required level of vitamin D (900 ICU/kg, NRC estimated requirement) and a high level of vitamin A (400,000 IU/kg) also developed severe lameness, growth depression and a rachiticlike condition, characterized by thicker than normal proximal tibial epiphyseal plates and lower than normal bone mineral content. When fed a diet containing the required level of vitamin A (4,000 IU/kg, NRC estimated requirement) and a high level of vitamin D (900,000 ICU/kg), poults developed hypervitaminosis D as evidenced by mild growth depression and renal tubular mineralization. When poults were fed a diet containing high levels of both vitamins A and D growth rate and bone mineral content were similar to control poults fed a diet containing the required levels of vitamins A and D. In addition, lameness and renal tubular mineralization were not apparent in the poults fed a diet containing high levels of both vitamins A and D. It was concluded that there is an antagonistic interaction between vitamins A and D.
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PMID:The interaction of dietary vitamin A and vitamin D related to skeletal development in the turkey poult. 400

In previous work we found that vitamin D-deficient and also calcium-deficient rats developed hypocalcemia and an impairment of bone formation and mineralization. The present study of thyroparathyroidectomized (TPTX) rats was undertaken to determine the effect of hypocalcemia without secondary hyperparathyroidism. TPTX rats fed a normal diet developed hypocalcemia and hyperphosphatemia in association with impairment of osteoblastic bone matrix formation and of mineralization of newly formed matrix. The serum calcium x phosphorus product was not decreased. The decreased formation was largely due to a reduction in matrix apposition indicating decreased synthetic activity of individual ostcoblasts. In contrast to the above results, when TPTX rats were fed a high-calcium diet to prevent hypocalcemia, no impairment of either formation or mineralization was found. From the results of these two experiments, it is reasonably certain that hypocalcemia was responsible for the inhibition of formation and mineralization. Moreover, based on the magnitude of the changes in serum calcium and bone parameters in TPTX rats, hypocalcemia could have accounted for the inhibition of formation and mineralization in calcium-deficient as well as vitamin D-deficient rats. In TPTX rats the mineralization defect was manifested by decreases in both the rate of osteoid maturation (indicating a delayed onset of mineralization) and the rate of mineralization. A strong correlation (r = 0.95, P < 0.001) was observed between these two rates suggesting a tight coupling of these two aspects of mineralization.TPTX rats also had lower bone resorption rates and higher serum phosphorus levels than sham-operated animals when the normal calcium diet was fed but not when the high-calcium diet was fed. Thus the inhibition of bone resorption in TPTX rats was at least partially prevented by correction of hyperphosphatemia. This is consistent with previous work showing an inverse relationship between serum phosphorus and bone resorption. Accordingly, the depression of bone resorption in TPTX rats was probably due to hyperphosphatemia as well as to hypoparathyroidism.
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PMID:Inhibition of bone matrix formation, mineralization, and resorption in thyroparathyroidectomized rats. 470 Apr 83

Rats fed a diet deficient in both vitamin D and Ca2+ exhibited a greater depression of the renal parathyroid hormone (PTH)-dependent adenylate cyclase than was observed in rats fed diets deficient in either vitamin D or calcium. Total serum Ca2+ was decreased from a control level of 11.2 mg/dl to 8.5 mg/dl in rats fed the diet deficient in calcium alone, and to 5.4 mg/dl in rats fed the diet deficient in vitamin D. Serum calcium was decreased further to 4.3 mg/dl in rats fed the diet deficient in both vitamin D and Ca2+. Serum immuno-reactive PTH was significantly elevated over control levels when rats were fed the test diets; however, there were no significant differences between the elevated levels in the three experimental groups. Repletion of rats deficient in vitamin D only with a single oral dose of 3200 I.U. vitamin D-2 resulted in restoration of serum calcium to normal levels, a return of serum PTH to the control state, and an associated increase in PTH-dependent adenylate cyclase activity to the control level by 72 h. Repletion of rats deficient in both vitamin D and Ca2+ with the same dose of vitamin D-2 raised serum Ca2+ to 7.2 mg/dl by 72 h, but did not cause a reduction in circulating PTH, nor did it result in any significant improvement in the responsiveness of the membrane adenylate cyclase to PTH. These results suggest that elevated PTH is a factor in the down regulation of the PTH-dependent adenylate cyclase, but do not rule out a role for calcium as a regulatory factor.
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PMID:Renal parathyroid hormone-dependent adenylate cyclase activity after repletion of vitamin D-deficient rats with vitamin D-2. 625 4

The effect of dietary phosphorus deficiency on the performance and on various parameters of calcium, phosphorus, and vitamin D metabolism was studied in laying hens. Phosphorus deficiency resulted in a decline in rate of production and egg weight, probably through appetite depression. The latter, or any secondary calcium deficiency, does not appear to cause the observed reduction in shell quality due to the deficiency. Similar to the response in the chick, phosphorus deficiency resulted in an increase in calcium-binding protein in intestine and kidney, there was no change in the activity of kidney 25-hydroxy-vitamin D3-1-hydroxylase. Percentages of calcium and phosphorus absorption were also higher during phosphorus deficiency. Medullary bone ash, decreased during phosphorus deficiency, was probably due to a reduction in the rate of bone formation.
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PMID:Egg shell quality, medullary bone ash, intestinal calcium and phosphorus absorption, and calcium-binding protein in phosphorus-deficient hens. 654 88

To examine the role of vitamin D in human phosphate absorption, we studied patients with chronic renal disease on hemodialysis, before and after correction of vitamin D deficiency. Thirty-centimeter segments of jejunum were perfused with test solutions containing varying concentrations of phosphate; phosphate absorption rate and electrical potential difference were measured. The data reveal that dialysis patients have depressed phosphate absorption, but the degree of this depression is modest, compared to the extent of their depressed calcium absorption. Therapy with 1,25-(OH)2D3 for 1 wk restored phosphate absorption rate to near normal. With or without 1,25-(OH)2D3 therapy, phosphate absorption was not influenced by calcium in the perfused test solutions. Examination of kinetic data suggests that the vitamin D deficiency of chronic renal failure causes a reduction by half in the rate of active phosphate absorption. By contrast, our data suggest that vitamin D deficiency does not alter passive phosphate absorption. By aspirating jejunal contents after ingestion of different foods, with and without aluminum hydroxide, the physiologic luminal phosphate concentration was found to vary between 0.7 and 12.2 mM. At the lower end of this range, phosphate absorption would be mediated entirely by active transport; at the higher phosphate concentrations, phosphate absorption would be mainly mediated by passive transport.
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PMID:Absorption of phosphate in the jejunum of patients with chronic renal failure before and after correction of vitamin D deficiency. 668 2


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