Effect of 24,25-dihydroxyvitamin D3 on 1,25-dihydroxyvitamin D3 metabolism in calcium-deficient rats

Matsumoto, Toshio; Yamato, Hideyuki; Morita, Keiko; Ezawa, Ikuko; Fukushima, Masafumi; Nishii, Yasuho; Ogata, Etsuro

doi:10.1042/bj2500671

Cited by 16 publications

(3 citation statements)

References 31 publications

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“…None of the factors regulating plasma 1,25(OH) 2 D 3 and 24,25(OH) 2 D 3 concentrations differed between groups except for vitamin D 3 intake (49). Thus, during positive Ca balance, high vitamin D 3 intake (as in the hVitD group) enhances 24-hydroxylase activity and results in enhanced production of 24,25(OH) 2 D 3 (11,12) and probably competitive inhibition of the synthesis of 1,25(OH) 2 D 3 from 25(OH)D 3 as has been suggested in Ca-deficient rats (50). Accordingly, between 10 and 13 wk of age in the hVitD group, plasma 24,25(OH) 2 D 3 concentrations started to increase, whereas plasma 1,25(OH) 2 D 3 concentrations were lower than in the cVitD group.…”

Section: Discussionmentioning

confidence: 71%

Moderate Cholecalciferol Supplementation Depresses Intestinal Calcium Absorption in Growing Dogs

Tryfonidou

Stevenhagen

Bemd

et al. 2002

The Journal of Nutrition

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Hormonal regulation of calcium (Ca) absorption was investigated in a cholecalciferol (vitamin D(3))-supplemented group (hVitD) vs. a control group (cVitD) of growing Great Danes (100 vs. 12.5 micro g vitamin D(3)/kg diet). Although Ca intakes did not differ, fractional Ca absorption was significantly lower in the hVitD group than in the cVitD group. There were no differences in plasma concentrations of Ca, inorganic phosphate, parathyroid hormone, growth hormone or insulin-like growth factor I between groups. Plasma 25-hydroxycholecalciferol [25(OH)D(3)] concentrations were maintained in the hVitD dogs at the same levels as in the cVitD dogs due to increased turnover of 25(OH)D(3) into 24,25-dihydroxycholecalciferol [24,25(OH)(2)D(3)] and 1,25-dihydroxycholecalciferol [1,25(OH)(2)D(3)]. In hVitD dogs, the greater plasma 24,25(OH)(2)D(3) concentration and the enhanced metabolic clearance rate (MCR) of 1,25(OH)(2)D(3) indicated upregulated 24-hydroxylase activity. The increased MCR of 1,25(OH)(2)D(3) decreased plasma 1,25(OH)(2)D(3) concentrations. In hVitD dogs, the greater production rate of 1,25(OH)(2)D(3) was consistent with the 12.9-fold greater renal 1alpha-hydroxylase gene expression compared with cVitD dogs and compensated to a certain extent for the accelerated MCR of 1,25(OH)(2)D(3). The moderately decreased plasma 1,25(OH)(2)D(3) concentration can only partially explain the decreased Ca absorption in the hVitD dogs. Intestinal vitamin D receptor concentrations did not differ between groups and did not account for the decreased Ca absorption. We suggest that 24,25(OH)(2)D(3) may downregulate Ca absorption.

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Section: Discussionmentioning

confidence: 71%

Moderate Cholecalciferol Supplementation Depresses Intestinal Calcium Absorption in Growing Dogs

Tryfonidou

Stevenhagen

Bemd

et al. 2002

The Journal of Nutrition

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“…Therefore, hypercalcemia concomitant with normal serum PTH levels may suppress 1a-hydroxylase, regardless of the presence or absence of CASR mutations. Moreover, according to previous works in animal models (41,42) 2 D. Finally, it cannot be excluded that the low levels of hCT found in FBH may play a role in the impairment of 1a-hydroxylase (27).…”

Section: Discussionmentioning

confidence: 99%

Different vitamin D substrate–product relationship after oral vitamin D supplementation in familial benign hypercalcemia, primary hyperparathyroidism, and healthy controls

Bevilacqua

Invernizzi

Righini³

et al. 2011

European Journal of Endocrinology

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Context: In healthy subjects and in patients with primary hyperparathyroidism (PH), the administration of a low dose of 25(OH)D (25 mg/day) increases the serum levels of both 25(OH)D and 1,25(OH) 2 D. It is unknown whether this relationship is present in patients affected by familial benign hypocalciuric hypercalcemia (FBH). Objective: To evaluate the different vitamin D substrate-product relationship after oral vitamin D supplementation in familial benign hypercalcemia, PH, and healthy controls. Design: We evaluated the main physiological regulators of 1a-hydroxylase and the substrate-product relationship of 25(OH)D and 1,25(OH) 2 D in 20 patients with PH, 25 with FBH, and 122 healthy sex-and age-matched controls before and after administration of 25(OH)D for 2 weeks. Results: 25(OH)D increased significantly in all subjects, whereas 1,25(OH) 2 D serum levels increased significantly in PH patients and healthy controls but not in patients with FBH. Therefore, a significant positive substrate-product relationship of 25(OH)D-1,25(OH) 2 D was found in PH and healthy controls, but not in FBH. Monomeric calcitonin (hCT-M) was significantly lower at baseline and after 25(OH)D supplementation in the FBH group compared with the other two groups. Conclusions: The lack of 1,25(OH) 2 D increase in FBH may be due to a direct inhibitory effect on 1a-hydroxylase of hypercalcemia per se, increased metabolic clearance of 1,25(OH) 2 D, or a decreased stimulus of 1a-hydroxylase related to persistently low levels of hCT.

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“…These two hydroxylase enzymes are reciprocally regulated, with 1␣-hydroxylase being directly responsive to a variety of regulators, including plasma levels of inorganic phosphate (P i ), growth hormone (GH), insulin-like growth factor I (IGF-I), and parathyroid hormone (PTH) [1][2][3]. Catabolism of 1,25(OH) 2 D 3 is mainly dependent upon 24-hydroxylase activity in the target organs of 1,25(OH) 2 D 3 and is regulated by 1,25(OH) 2 D 3 itself [4], P [5], 24,25(OH) 2 D 3 [6,7], PTH [8], and possibly by GH and IGF-I [9]. The general consensus is that pharmacological GH excess is accompanied by an increase in plasma 1,25(OH) 2 D 3 levels [10,11] due to stimulation of the renal production of 1,25(OH) 2 D 3 by IGF-I [2].…”

Section: Introductionmentioning

confidence: 99%

Different effects of physiologically and pharmacologically increased growth hormone levels on cholecalciferol metabolism at prepubertal age

Tryfonidou

Hazewinkel

2004

The Journal of Steroid Biochemistry and Molecular Biology

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Effect of 24,25-dihydroxyvitamin D3 on 1,25-dihydroxyvitamin D3 metabolism in calcium-deficient rats

Cited by 16 publications

References 31 publications

Moderate Cholecalciferol Supplementation Depresses Intestinal Calcium Absorption in Growing Dogs

Moderate Cholecalciferol Supplementation Depresses Intestinal Calcium Absorption in Growing Dogs

Different vitamin D substrate–product relationship after oral vitamin D supplementation in familial benign hypercalcemia, primary hyperparathyroidism, and healthy controls

Different effects of physiologically and pharmacologically increased growth hormone levels on cholecalciferol metabolism at prepubertal age

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