Interaction between Vitamin D and calcium
Abstract A low calcium intake aggravates the consequences of vitamin D deficiency. This suggests an interaction between vitamin D and calcium intake, which is the subject of this review. The active vitamin D metabolite, 1,25-dihydroxyvitamin D (1,25(OH)2D) binds to the vitamin D receptor (VDR) in th...
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| Veröffentlicht in: | Scandinavian journal of clinical & laboratory investigation. Supplement Jg. 72; H. S243; S. 60 - 64 |
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| Sprache: | Englisch |
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Colchester
Informa Healthcare
01.04.2012
Taylor & Francis Informa |
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| ISSN: | 0036-5513, 2166-1030, 1502-7686, 2166-1030 |
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| Abstract | Abstract
A low calcium intake aggravates the consequences of vitamin D deficiency. This suggests an interaction between vitamin D and calcium intake, which is the subject of this review. The active vitamin D metabolite, 1,25-dihydroxyvitamin D (1,25(OH)2D) binds to the vitamin D receptor (VDR) in the intestinal cell and stimulates the active calcium transport from the intestine to the circulation. Vitamin D is not needed for the paracellular transport of calcium, which depends on the calcium gradient. Active calcium absorption decreases when the serum 25-hydroxyvitamin D (25(OH)D) concentration is < 20 nmol/L. Studies in the VDR null mouse have demonstrated that bone mineralisation can be restored without vitamin D by a diet very high in calcium and lactose. Both calcium and vitamin D metabolites can decrease the secretion of parathyroid hormone (PTH) through the calcium sensing receptor and the VDR respectively. With an increasing serum 25(OH)D concentration up to 100 nmol/L or higher serum PTH is still decreasing. A high calcium intake increases the half life of 25(OH)D. In patients with primary or secondary hyperparathyroidism, the half life of 25(OH)D is shorter. Similar interactions between calcium intake and vitamin D status have been shown in rat experiments, generally indicating that a high calcium intake is good for the vitamin D economy. Clinical trials with vitamin D and/or calcium to decrease fracture incidence generally have shown that trials with vitamin D and calcium had better results than calcium or vitamin D alone. The effects of these trials also depend on baseline calcium intake, baseline vitamin D status, age and residence. Trials in institutionalized persons had better results than in independently living elderly. These results confirm that an interaction exists between calcium and vitamin D. |
|---|---|
| AbstractList | A low calcium intake aggravates the consequences of vitamin D deficiency. This suggests an interaction between vitamin D and calcium intake, which is the subject of this review. The active vitamin D metabolite, 1,25-dihydroxyvitamin D (1,25(OH)
2
D) binds to the vitamin D receptor (VDR) in the intestinal cell and stimulates the active calcium transport from the intestine to the circulation. Vitamin D is not needed for the paracellular transport of calcium, which depends on the calcium gradient. Active calcium absorption decreases when the serum 25-hydroxyvitamin D (25(OH)D) concentration is < 20 nmol/L. Studies in the VDR null mouse have demonstrated that bone mineralisation can be restored without vitamin D by a diet very high in calcium and lactose. Both calcium and vitamin D metabolites can decrease the secretion of parathyroid hormone (PTH) through the calcium sensing receptor and the VDR respectively. With an increasing serum 25(OH)D concentration up to 100 nmol/L or higher serum PTH is still decreasing. A high calcium intake increases the half life of 25(OH)D. In patients with primary or secondary hyperparathyroidism, the half life of 25(OH)D is shorter. Similar interactions between calcium intake and vitamin D status have been shown in rat experiments, generally indicating that a high calcium intake is good for the vitamin D economy. Clinical trials with vitamin D and/or calcium to decrease fracture incidence generally have shown that trials with vitamin D and calcium had better results than calcium or vitamin D alone. The effects of these trials also depend on baseline calcium intake, baseline vitamin D status, age and residence. Trials in institutionalized persons had better results than in independently living elderly. These results confirm that an interaction exists between calcium and vitamin D. Abstract A low calcium intake aggravates the consequences of vitamin D deficiency. This suggests an interaction between vitamin D and calcium intake, which is the subject of this review. The active vitamin D metabolite, 1,25-dihydroxyvitamin D (1,25(OH)2D) binds to the vitamin D receptor (VDR) in the intestinal cell and stimulates the active calcium transport from the intestine to the circulation. Vitamin D is not needed for the paracellular transport of calcium, which depends on the calcium gradient. Active calcium absorption decreases when the serum 25-hydroxyvitamin D (25(OH)D) concentration is < 20 nmol/L. Studies in the VDR null mouse have demonstrated that bone mineralisation can be restored without vitamin D by a diet very high in calcium and lactose. Both calcium and vitamin D metabolites can decrease the secretion of parathyroid hormone (PTH) through the calcium sensing receptor and the VDR respectively. With an increasing serum 25(OH)D concentration up to 100 nmol/L or higher serum PTH is still decreasing. A high calcium intake increases the half life of 25(OH)D. In patients with primary or secondary hyperparathyroidism, the half life of 25(OH)D is shorter. Similar interactions between calcium intake and vitamin D status have been shown in rat experiments, generally indicating that a high calcium intake is good for the vitamin D economy. Clinical trials with vitamin D and/or calcium to decrease fracture incidence generally have shown that trials with vitamin D and calcium had better results than calcium or vitamin D alone. The effects of these trials also depend on baseline calcium intake, baseline vitamin D status, age and residence. Trials in institutionalized persons had better results than in independently living elderly. These results confirm that an interaction exists between calcium and vitamin D. A low calcium intake aggravates the consequences of vitamin D deficiency. This suggests an interaction between vitamin D and calcium intake, which is the subject of this review. The active vitamin D metabolite, 1,25-dihydroxyvitamin D (1,25(OH)(2)D) binds to the vitamin D receptor (VDR) in the intestinal cell and stimulates the active calcium transport from the intestine to the circulation. Vitamin D is not needed for the paracellular transport of calcium, which depends on the calcium gradient. Active calcium absorption decreases when the serum 25-hydroxyvitamin D (25(OH)D) concentration is < 20 nmol/L. Studies in the VDR null mouse have demonstrated that bone mineralisation can be restored without vitamin D by a diet very high in calcium and lactose. Both calcium and vitamin D metabolites can decrease the secretion of parathyroid hormone (PTH) through the calcium sensing receptor and the VDR respectively. With an increasing serum 25(OH)D concentration up to 100 nmol/L or higher serum PTH is still decreasing. A high calcium intake increases the half life of 25(OH)D. In patients with primary or secondary hyperparathyroidism, the half life of 25(OH)D is shorter. Similar interactions between calcium intake and vitamin D status have been shown in rat experiments, generally indicating that a high calcium intake is good for the vitamin D economy. Clinical trials with vitamin D and/or calcium to decrease fracture incidence generally have shown that trials with vitamin D and calcium had better results than calcium or vitamin D alone. The effects of these trials also depend on baseline calcium intake, baseline vitamin D status, age and residence. Trials in institutionalized persons had better results than in independently living elderly. These results confirm that an interaction exists between calcium and vitamin D. A low calcium intake aggravates the consequences of vitamin D deficiency. This suggests an interaction between vitamin D and calcium intake, which is the subject of this review. The active vitamin D metabolite, 1,25-dihydroxyvitamin D (1,25(OH)(2)D) binds to the vitamin D receptor (VDR) in the intestinal cell and stimulates the active calcium transport from the intestine to the circulation. Vitamin D is not needed for the paracellular transport of calcium, which depends on the calcium gradient. Active calcium absorption decreases when the serum 25-hydroxyvitamin D (25(OH)D) concentration is < 20 nmol/L. Studies in the VDR null mouse have demonstrated that bone mineralisation can be restored without vitamin D by a diet very high in calcium and lactose. Both calcium and vitamin D metabolites can decrease the secretion of parathyroid hormone (PTH) through the calcium sensing receptor and the VDR respectively. With an increasing serum 25(OH)D concentration up to 100 nmol/L or higher serum PTH is still decreasing. A high calcium intake increases the half life of 25(OH)D. In patients with primary or secondary hyperparathyroidism, the half life of 25(OH)D is shorter. Similar interactions between calcium intake and vitamin D status have been shown in rat experiments, generally indicating that a high calcium intake is good for the vitamin D economy. Clinical trials with vitamin D and/or calcium to decrease fracture incidence generally have shown that trials with vitamin D and calcium had better results than calcium or vitamin D alone. The effects of these trials also depend on baseline calcium intake, baseline vitamin D status, age and residence. Trials in institutionalized persons had better results than in independently living elderly. These results confirm that an interaction exists between calcium and vitamin D.A low calcium intake aggravates the consequences of vitamin D deficiency. This suggests an interaction between vitamin D and calcium intake, which is the subject of this review. The active vitamin D metabolite, 1,25-dihydroxyvitamin D (1,25(OH)(2)D) binds to the vitamin D receptor (VDR) in the intestinal cell and stimulates the active calcium transport from the intestine to the circulation. Vitamin D is not needed for the paracellular transport of calcium, which depends on the calcium gradient. Active calcium absorption decreases when the serum 25-hydroxyvitamin D (25(OH)D) concentration is < 20 nmol/L. Studies in the VDR null mouse have demonstrated that bone mineralisation can be restored without vitamin D by a diet very high in calcium and lactose. Both calcium and vitamin D metabolites can decrease the secretion of parathyroid hormone (PTH) through the calcium sensing receptor and the VDR respectively. With an increasing serum 25(OH)D concentration up to 100 nmol/L or higher serum PTH is still decreasing. A high calcium intake increases the half life of 25(OH)D. In patients with primary or secondary hyperparathyroidism, the half life of 25(OH)D is shorter. Similar interactions between calcium intake and vitamin D status have been shown in rat experiments, generally indicating that a high calcium intake is good for the vitamin D economy. Clinical trials with vitamin D and/or calcium to decrease fracture incidence generally have shown that trials with vitamin D and calcium had better results than calcium or vitamin D alone. The effects of these trials also depend on baseline calcium intake, baseline vitamin D status, age and residence. Trials in institutionalized persons had better results than in independently living elderly. These results confirm that an interaction exists between calcium and vitamin D. |
| Author | Lips, Paul |
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A low calcium intake aggravates the consequences of vitamin D deficiency. This suggests an interaction between vitamin D and calcium intake, which is... A low calcium intake aggravates the consequences of vitamin D deficiency. This suggests an interaction between vitamin D and calcium intake, which is the... |
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| SubjectTerms | Absorption Animals Biological and medical sciences Calcium - metabolism Calcium, Dietary - administration & dosage Clinical Trials as Topic Humans Hyperparathyroidism, Secondary - prevention & control Investigative techniques, diagnostic techniques (general aspects) Medical sciences Mice Vitamin D - analogs & derivatives Vitamin D - blood Vitamin D - metabolism |
| Title | Interaction between Vitamin D and calcium |
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