Effects of Vitamin D3 Metabolites in Ovariectomized Rats

1989 ◽  
Vol 17 (3) ◽  
pp. 243-248
Author(s):  
H. Orimo ◽  
C. Tsutsumi ◽  
N. Hosoya ◽  
Y. Maeda ◽  
H. Yamato ◽  
...  

The effects of two vitamin D3 metabolites, 24 R,25-dihydroxyvitamin D3 and lα,25-dihydroxyvitamin D3, were investigated in ovariectomized rats. The amount of ash in the femur on a defatted dry weight basis was significantly greater in rats treated with 1 μg/kg 24 R,25-dihydroxyvitamin D3, or 0.01 or 0.1 μg/kg lα,25-dihydroxyvitamin D3 than in the controls. The concentration of bone gla protein in serum and amounts in the femur were significantly greater in rats treated with 1 or 10 Mg/kg 24 R,25-dihydroxyvitamin D3, but not those given 1α,25-dihydroxyvitamin D3 compared with the controls. These results suggest that 24 R,25-dihydroxyvitamin D3 increased bone mass probably through the stimulation of bone formation.

2018 ◽  
Vol 18 (2) ◽  
pp. 206-210 ◽  
Author(s):  
Mehmet Dagli ◽  
Ali Kutlucan ◽  
Sedat Abusoglu ◽  
Abdulkadir Basturk ◽  
Mehmet Sozen ◽  
...  

A decrease in bone mass is observed in hemophilic patients. The aim of this study was to evaluate bone mineral density (BMD), parathyroid hormone (PTH), 25-hydroxy vitamin D (vitamin D), and a bone formation and resorption marker, procollagen type I N-terminal propeptide (PINP) and urinary N-terminal telopeptide (uNTX) respectively, in hemophilic patients and healthy controls. Laboratory parameters related to the pathogenesis of bone loss such as neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio (PLR) were also evaluated. Thirty-five men over 18 years of age, with severe hemophilia (A and B) and receiving secondary prophylaxis, were included in the study. The same number of age-, sex-, and ethnicity-matched healthy controls were evaluated. Anthropometric, biochemical, and hormonal parameters were determined in both groups. No significant difference in anthropometric parameters was found between the two groups. The BMD was low in 34% of hemophilic patients. Vitamin D, calcium, and free testosterone levels were significantly lower (p < 0.001, p = 0.011, p < 0.001, respectively), while PTH, PINP, and activated partial thromboplastin time (aPTT) levels were significantly higher (p < 0.014, p = 0.043, p < 0.001, respectively), in hemophilic patients compared to controls. There was no significant difference between the two groups in NLR, PLR, phosphorus, thyroid-stimulating hormone, and uNTX level. The reduction of bone mass in hemophilic patients may be evaluated using the markers of bone formation and resorption, enabling early detection and timely treatment.


1997 ◽  
Vol 12 (4) ◽  
pp. 590-597 ◽  
Author(s):  
Hiroaki Fuse ◽  
Seiji Fukumoto ◽  
Hideyuki Sone ◽  
Yoshiko Miyata ◽  
Tomoyuki Saito ◽  
...  

1986 ◽  
Vol 251 (4) ◽  
pp. E400-E406 ◽  
Author(s):  
P. J. Marie ◽  
L. Cancela ◽  
N. Le Boulch ◽  
L. Miravet

The effects of pregnancy and lactation on endosteal bone formation and resorption were evaluated in vitamin D-depleted (-D) and vitamin D-repleted (+D) rats. Pregnancy induced a marked stimulation of osteoclastic bone resorption and of static and dynamic parameters of bone formation and mineralization. Bone resorption increased independently of vitamin D status and did not correlate with plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D] levels, but it was associated with increased plasma immunoreactive parathyroid hormone (iPTH) concentrations. Stimulation of the endosteal bone formation rate was mainly impaired in D-depleted rats, resulting in trabecular bone loss, which, in -D mother rats, was associated with decreased bone ash and total bone calcium. Lactation further stimulated bone resorption and reduced the trabecular bone volume; ash weight and bone calcium content were also decreased independently of the vitamin D status and changes in plasma iPTH levels. In presence of vitamin D, the bone formation rate increased fourfold during lactation but was unchanged in -D lactating rats. During lactation, vitamin D-depleted rats lost twofold more calcified bone than +D rats because of impaired mineralization. Thus, the present study shows that both the endosteal bone resorption and formation are stimulated by pregnancy and lactation and that vitamin D is required for normal bone mineralization during the reproductive period.


2005 ◽  
Vol 20 (10) ◽  
pp. 1742-1755 ◽  
Author(s):  
Hua Zhu Ke ◽  
Hong Qi ◽  
D Todd Crawford ◽  
Hollis A Simmons ◽  
Gang Xu ◽  
...  

Nature ◽  
1978 ◽  
Vol 276 (5687) ◽  
pp. 517-519 ◽  
Author(s):  
A. ORNOY ◽  
D. GOODWIN ◽  
D. NOFF ◽  
S. EDELSTEIN

2006 ◽  
Vol 16 (7) ◽  
pp. 1799-1802 ◽  
Author(s):  
Kimberly O. Cameron ◽  
Bruce A. Lefker ◽  
Margaret Y. Chu-Moyer ◽  
David T. Crawford ◽  
Paul DaSilva Jardine ◽  
...  

1985 ◽  
Vol 109 (2) ◽  
pp. 243-248 ◽  
Author(s):  
Nirandon Wongsurawat ◽  
H. James Armbrecht

Abstract. Previous studies have shown that there is an impairment in renal production of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the major biologically active metabolite of vitamin D3, in diabetes. This impairment is not due to a deficiency in the parathyroid hormone (PTH), a major stimulator of renal 1,25(OH)2D3 production. Therefore, we have investigated the capacity of PTH to stimulate 1,25(OH)2D3 production in insulin deficiency and with insulin replacement. Experiments were performed in rats fed a 0.6% calcium, vitamin D sufficient diet for 2 weeks. Thyroparathyroidectomy was performed on all rats. Rats to be rendered diabetic were injected with streptozotocin immediately after surgery. In non-diabetic rats, PTH administration significantly increased renal 1,25(OH)2D3 production (11 ± 2 vs 46 ± 5 pg/min/g; P < 0.05). In diabetic rats, however, PTH caused only a modest increase in 1,25(OH)2D3 production (11 ± 1 vs 19 ± 4 pg/min/g; P < 0.05). With insulin replacement, PTH stimulation of 1,25(OH)2D3 production was markedly increased over that seen in diabetic rats (48 ± 12 vs 19 ± 4 pg/min/g; P < 0.05). PTH was equally effective in raising serum calcium, depressing serum phosphorus and tubular reabsorption of phosphate in non-diabetic as well as in diabetic rats. These results demonstrate that insulin is necessary for the maximal stimulation of renal 1,25(OH)2D3 production by PTH. However, insulin is not necessary for PTH action in terms of renal handling of phosphate and inducing hypercalcaemia. These results suggest multiple pathways for the action of PTH, only some of which are insulin requiring.


2015 ◽  
Vol 29 (12) ◽  
pp. 1950-1955 ◽  
Author(s):  
Yuko Morii ◽  
Hiroshi Matsushita ◽  
Akira Minami ◽  
Hiroaki Kanazawa ◽  
Takashi Suzuki ◽  
...  

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