Effect of Vitamin D Metabolites on Bone Metabolism in a Rat Model of Postmenopausal Osteoporosis

Matsumoto, Toshio; Ezawa, Ikuko; Morita, Keiko; Kawanobe, Yumiko; Ogata, Etsuro

doi:10.3177/jnsv.31.supplement_s61

Cited by 20 publications

(7 citation statements)

References 14 publications

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“…Already in 1980 it was shown that 24,25D3 directly stimulates calcification of bone in interaction with PTH and that the number and size of resorption sites in bone is decreased by 24,25D3 (Endo et al, 1980; Galus et al, 1980). Several other studies supported a positive effect of 24,25D3 on bone metabolism (Matsumoto et al, 1985; Tam et al, 1986; Kato et al, 1998) while one study showed no effect of 24,25D3 on histomorphometric parameters in ovariectomized rats (Erben et al, 1992). Administration of 24,25D3 in combination with 1,25D3 improved fracture healing in chickens (Seo et al, 1997) and interestingly, 24,25D3 serum levels correlated to fracture healing (Seo and Norman, 1997).…”

Section: Vitamin D Bone Metabolism and Osteoblastmentioning

confidence: 91%

Vitamin D and gene networks in human osteoblasts

Peppel¹,

Leeuwen²

2014

Front. Physiol.

110

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Bone formation is indirectly influenced by 1,25-dihydroxyvitamin D3 (1,25D3) through the stimulation of calcium uptake in the intestine and re-absorption in the kidneys. Direct effects on osteoblasts and bone formation have also been established. The vitamin D receptor (VDR) is expressed in osteoblasts and 1,25D3 modifies gene expression of various osteoblast differentiation and mineralization-related genes, such as alkaline phosphatase (ALPL), osteocalcin (BGLAP), and osteopontin (SPP1). 1,25D3 is known to stimulate mineralization of human osteoblasts in vitro, and recently it was shown that 1,25D3 induces mineralization via effects in the period preceding mineralization during the pre-mineralization period. For a full understanding of the action of 1,25D3 in osteoblasts it is important to get an integrated network view of the 1,25D3-regulated genes during osteoblast differentiation and mineralization. The current data will be presented and discussed alluding to future studies to fully delineate the 1,25D3 action in osteoblast. Describing and understanding the vitamin D regulatory networks and identifying the dominant players in these networks may help develop novel (personalized) vitamin D-based treatments. The following topics will be discussed in this overview: (1) Bone metabolism and osteoblasts, (2) Vitamin D, bone metabolism and osteoblast function, (3) Vitamin D induced transcriptional networks in the context of osteoblast differentiation and bone formation.

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Section: Vitamin D Bone Metabolism and Osteoblastmentioning

confidence: 91%

Vitamin D and gene networks in human osteoblasts

Peppel¹,

Leeuwen²

2014

Front. Physiol.

110

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“…dosage of vitamin D3 in cotton-seed oil was supplied every other day throughout the experimental period. During the last 4 weeks 24,25(OH)2D3-treated groups of rats were given 1, 5 or 10 jug of 24,25(OH)2D3/100 g per day (Kureha Chemical Co., Tokyo, Japan) in medium-chain triacylglycerols orally every day (Matsumoto et al, 1985). The control group of rats received the vehicle alone.…”

Section: Materials and Methods Animals And Dietmentioning

confidence: 99%

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

Matsumoto

Yamato

Morita

et al. 1988

Biochemical Journal

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The effect of 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] on 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] metabolism was examined in rats fed on a low-calcium diet. These rats exhibit hypocalcaemia, high urinary cyclic AMP excretion, a markedly elevated serum 1,25(OH)2D concentration and low serum concentrations of both 24,25(OH)2D and 25(OH)D. When the rats are treated orally with 1, 5 or 10 micrograms of 24,25(OH)2D3/100 g every day, there is a dramatic decrease in serum 1,25(OH)2D concentration in a dose-dependent manner concomitant with an increase in serum 24,25(OH)2D concentration. Serum calcium concentration and urinary cyclic AMP excretion are not significantly affected by the 24,25(OH)2D3 treatment, which suggests that parathyroid function is not affected by the 24,25(OH)2D3 treatment. The 25(OH)D3 1 alpha-hydroxylase activity measured in kidney homogenates is markedly elevated in rats on a low-calcium diet but is not affected by any doses of 24,25(OH)2D3. In contrast, recovery of intravenously injected [3H]1,25(OH)2D3 in the serum is decreased in 24,25(OH)2D3-treated rats. Furthermore, when [3H]1,25(OH)2D3 is incubated in vitro with kidney or intestinal homogenates of 24,25(OH)2D3-treated rats there is a decrease in the recovery of radioactivity in the total lipid extract as well as in the 1,25(OH)2D3 fraction along with an increase in the recovery of radioactivity in the water-soluble phase. These results are consistent with the possibility that 24,25(OH)2D3 has an effect on 1,25(OH)2D3 metabolism, namely that of enhancing the degradation of 1,25(OH)2D3. However, because a considerable proportion of the injected 24,25(OH)2D3 is expected to be converted into 1,24,25(OH)3D3 by renal 1 alpha-hydroxylase in 24,25(OH)2D3-treated rats, at least a part of the decrease in serum 1,25(OH)2D concentration may be due to a competitive inhibition by 24,25(OH)2D3 of the synthesis of 1,25(OH)2D3 from 25(OH)D3. Thus the physiological importance of the role of 24,25(OH)2D3 in regulating the serum 1,25(OH)2D concentration as well as the mechanism and metabolic pathway of degradation of 1,25(OH)2D3 remain to be clarified.

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“…This system is a good model for such clinical cases. On the other hand, 24/?,25(OH)2D3 was re ported to stimulate the growth of cartilage or chon drocytes [2,4,11,12] essential for bone formation [5], to stimulate the formation of osteocalcin which is associated with bone formation [15] and to improve the lowered bone strength of ovariectomized rats which had been raised on a low calcium diet [7], We believed that K-DR would improve the lowered bone strength in mice with Lewis lung carcinoma, and the results were as expected. It was also reported that a receptor specific to 24/?,25(OH)2D3 was found in the long bone of newborn rats [13],…”

Section: Discussionmentioning

confidence: 99%

“…In such a system la,25-dihydroxyvitamin D3, which is considered to be an active form of vitamin D3, did not increase bone strength [7], On the other hand it is well known that cancer patients with bone metastasis or osteosarcoma which cause abnormal calcium metabolism suffer from bone fracture due to a decrease in bone strength.…”

Section: Introductionmentioning

confidence: 99%