scholarly journals More Than Bone Health: The Many Roles for Vitamin D

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2388
Author(s):  
Emma Beckett

Vitamin D is well known for its important roles in maintaining calcium homeostasis and bone mineralization via the regulation of calcium mobilization and renal reabsorption, and the intestinal absorption of both calcium and phosphorus [...]

JMS SKIMS ◽  
2011 ◽  
Vol 14 (2) ◽  
pp. 40-42
Author(s):  
Muzafar Maqsood Wani ◽  
Imtiaz Ahmed Wani

Major biologic function of activated vitamin D is to maintain normal blood levels of calcium and phosphorus, thus regulating bone mineralization. Research suggests that vitamin D may help in immunomodulation, regulating cell growth and 1,4 differentiation as well as some diverse unspecified functions. Overt vitamin D deficiency leads to hypocalcaemia, secondary hyperparathyroidism and increased bone turnover, which in prolonged and severe cases may cause rickets in children and osteomalacia in elderly.... JMS 2011;14(2):40-42


2012 ◽  
Vol 92 (1) ◽  
pp. 131-155 ◽  
Author(s):  
Aline Martin ◽  
Valentin David ◽  
L. Darryl Quarles

Calcium (Ca2+) and phosphate (PO43−) homeostasis are coordinated by systemic and local factors that regulate intestinal absorption, influx and efflux from bone, and kidney excretion and reabsorption of these ions through a complex hormonal network. Traditionally, the parathyroid hormone (PTH)/vitamin D axis provided the conceptual framework to understand mineral metabolism. PTH secreted by the parathyroid gland in response to hypocalcemia functions to maintain serum Ca2+ levels by increasing Ca2+ reabsorption and 1,25-dihydroxyvitamin D [1,25(OH)2D] production by the kidney, enhancing Ca2+ and PO43− intestinal absorption and increasing Ca2+ and PO43− efflux from bone, while maintaining neutral phosphate balance through phosphaturic effects. FGF23 is a recently discovered hormone, predominately produced by osteoblasts/osteocytes, whose major functions are to inhibit renal tubular phosphate reabsorption and suppress circulating 1,25(OH)2D levels by decreasing Cyp27b1-mediated formation and stimulating Cyp24-mediated catabolism of 1,25(OH)2D. FGF23 participates in a new bone/kidney axis that protects the organism from excess vitamin D and coordinates renal PO43− handling with bone mineralization/turnover. Abnormalities of FGF23 production underlie many inherited and acquired disorders of phosphate homeostasis. This review discusses the known and emerging functions of FGF23, its regulation in response to systemic and local signals, as well as the implications of FGF23 in different pathological and physiological contexts.


1980 ◽  
Vol 239 (6) ◽  
pp. G480-G484 ◽  
Author(s):  
U. Gafter ◽  
J. A. Kraut ◽  
D. B. Lee ◽  
V. Silis ◽  
M. W. Walling ◽  
...  

To investigate the effect of metabolic acidosis on intestinal calcium (Ca) and phosphorus (P) absorption and vitamin D metabolism, metabolic balance studies and in vitro gut sac uptake of 45Ca and [32P]phosphate were performed in rats maintained on low-Ca and moderately low-P diet and fed NH4Cl for 3 or 9 days and pair-fed controls. Plasma 1,25(OH)2D concentration was measured in the rats fed NH4Cl for 9 days and their controls. Net Ca and P absorption was 87–92% in the acidotic rats and did not differ from control. Moreover, gut sac uptakes of 45Ca and [32P]phosphate were not different from control. Plasma 1,25(OH)2D was higher in the ammonium chloride-fed rats than in controls (213 +/- 44 vs. 110 +/- 12 pg/ml), and serum P was lower in the acidotic animals (4.6 +/- 0.7 vs. 7.6 +/- 0.3 mg/dl). These data indicate that metabolic acidosis does not depress the augmented intestinal absorption of calcium and phosphorus noted during their dietary deprivation nor reduce the plasma level of 1,25(OH)2D.


1975 ◽  
Vol 42 (1) ◽  
pp. 1-9 ◽  
Author(s):  
M. Teotia ◽  
S. P. S. Teotia ◽  
T. Raman ◽  
N. L. Sharma ◽  
R. K. Singh

2019 ◽  
Vol 6 (2) ◽  
pp. 549
Author(s):  
Madhu P. K. ◽  
Bhagwan B.

Background: β-Thalassemia major is a serious hematological problem requiring regular blood transfusions. In regularly transfused thalassemic patients, metabolic bone disease is an important cause of morbidity. Problems include bone pain, deformities, short stature, osteopenia/osteoporosis, rickets, osteomalacia, spinal deformities, nerve compression and fractures. This study was undertaken to evaluate the status of bone health in children with β-thalassemia major by selected biochemical indices and radiological examination.Methods: Fifty children with β- thalassemia major were enrolled. Detailed history, examination and anthropometry were done. Serum calcium, phosphorus, magnesium, alkaline phosphatase, and vitamin D levels were measured. X-ray of skull, wrist, and knee were studied for radiological changes. Biochemical indices were analysed with appropriate statistical tests.Results: Stunting and wasting was observed in 58% and 44% children respectively. Hypocalcaemia was seen in 22%, hyperphosphatemia in 56% and 24% children had raised alkaline phosphatase levels. Vitamin D levels were severely deficient in 12%, deficient in 50%, and insufficient in 38% of children. There was no significant difference between vitamin D levels of cases and controls. Radiologically almost all children had a range of osteopathy, like thinned out cortex (96%), medullary expansion (54%), loss of density (40%), diffuse osteoporosis (18%) and growth arrest lines were seen in 8% children.Conclusions: Vitamin D abnormalities and radiological features suggestive of decreased bone mineralization are seen in all the children with β-thalassemia major treated with periodic blood transfusion at this institute. No biochemical predictors of bone disease in these children were identified. 


1985 ◽  
Vol 68 (1) ◽  
pp. 97-100 ◽  
Author(s):  
U. Gafter ◽  
S. Edelstein ◽  
J. Levi

1. The effect of bicarbonate (NaHCO3) feeding on intestinal absorption of calcium and phosphorus and vitamin D metabolism was investigated. Gut sac uptake of 45Ca and [32P]phosphate in vitro, as well as the plasma level of vitamin D metabolites, was determined in rats fed with NaHCO3 for 9 days and their pair-fed controls. 2. Duodenal uptake of 45Ca and [32P]phosphate by alkalotic rats was less than duodenal uptake by controls. 1,25(OH)2D plasma level was much higher in alkalotic rats than in their controls, and 25(OH)D slightly higher than in controls. 3. These data suggest that NaHCO3 feeding causes a substantial increase in 1,25(OH)2D plasma level, but interferes with calcium and phosphorus absorption in the duodenum.


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