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1.
Toshio Okano Tamiko Kimura Naoko Tsugawa Yukiko Oshio Yumiko Teraoka Tadashi Kobayashi 《Journal of bone and mineral metabolism》1993,11(2):S23-S32
Bioavailability of calcium (Ca) from oyster shell electrolysate (Active Absorbable Ca: AACa) and DL-Ca lactate in rats was
investigated. Plasma Ca metabolism, bone mineral density and vitamin D-deficient rats were measured and compared each other.
Vitamin D-deficient rats were fedad libitum a vitamin D-free diet containing 0.44 % Ca or 1.20 % Ca adjusted with either AACa or DL-Ca lactate with or without oral supplementation
of physiological dose (10 IU/rat/day) of vitamin D3 for 28 days. During and after feeding, concentrations of Ca, phosphorus, parathyroid hormone (PTH), 25-hydroxyvitamin D3 (25-OH-D3), 1α, 25-dihydroxyvitamin D3 [1, 25(OH)2D3] and alkaline phosphatase (Alp) activity in plasma were measured. Furthermore, femoral Ca and phosphorus contents, mineral
density and mechanical strength were also measured. Despite of the differences of contents and chemical forms of Ca in diets,
all the groups showed prompt and complete recoveries in both Ca and vitamin D malnutritions under vitamin D-replete condition
and there was no significant difference among all the groups in increases of body weight gains and plasma Ca levels, and in
decreases of plasma PTH level and Alp activity. In contrast, the groups fed the same diets under vitamin D-deficient condition
showed no significant recoveries in both plasma Ca metabolism and bone mineralization although Ca bioavailability of AACa
appeared to be slightly better than that of DL-Ca lactate. These results suggest that bioavailability of Ca from AACa and
DL-Ca lactate are substantially equal in increasing plasma Ca levels, bone mineral density and mechanical strength in both
vitamin D-replete and vitamin D-deficient rats. 相似文献
2.
Naoko Tsugawa Toshio Okano Sonoko Masuda Tadashi Kobayashi Noboru Kubodera Katsuhiko Sato Yasuho Nishii 《Journal of bone and mineral metabolism》1994,12(Z1):S13-S17
22-Oxa-1α, 25-dihydroxyvitamin D3 (OCT) and 2β-(3-Hydroxypropoxy)-1α, 25-dihydroxyvitamin D3 (ED-71) are novel synthetic vitamin D3 analogues. In order to examine their calcemic actions on intestine and bone, we have investigated the effects of OCT and
ED-71 on intestinal Ca transport, bone mobilization and plasma parathyroid hormone (PTH) level in vitamin D-deficient rats.
The vitamin D-deficient rats were intravenously given either 6.25μg/kg or 0.2μg/kg of 1,25-D3, OCT or ED-71 and theirplasma Ca levels and intestinal Ca transport were measured periodically. At a high dose, 1,25(OH)2D3 and ED-71 showed a strong biphasic stimulation of intestinal Ca transport and bone mobilization, and reduced the plasma PTH
levels to the normal level completely. On the other hand, OCT failed to suppress the PTH secretion although it exerted first
phase action on the both intestinal Ca transport and bone mobilization in vitamin D-deficient rats. The reason why OCT failed
to suppress the PTH secretion even at a high dose, has not yet been clarified, but it may be at least in part due to its weak
calcemic action and short half-life in plasma. 相似文献
3.
Ryo Okazaki Toshitsugu Sugimoto Hiroshi Kaji Yoshio Fujii Masataka Shiraki Daisuke Inoue Itsuro Endo Toshio Okano Takako Hirota Issei Kurahashi Toshio Matsumoto 《Journal of bone and mineral metabolism》2011,29(1):103-110
Vitamin D insufficiency is a risk for both skeletal and nonskeletal health. However, some ambiguity remains about threshold serum 25(OH)D for vitamin D insufficiency. To determine the threshold serum 25(OH)D to maintain normal calcium availability without elevation in serum parathyroid hormone (PTH) among Japanese subjects with various calcium intakes, we conducted a multicenter prospective open-labeled study. We recruited 107 ambulatory subjects without disorders affecting vitamin D metabolism to whom oral vitamin D3 800?IU/day for 4?weeks or 1,200?IU/day for 8?weeks was given. Serum 25(OH)D, PTH, calcium, phosphate, and magnesium were measured before and after vitamin D3 supplementation. Calcium intake was assessed by questionnaires. When all the data were combined, serum 25(OH)D was negatively correlated with PTH. The cubic spline curve between serum 25(OH)D and PTH indicated PTH reached its plateau between 35 and 40?pg/ml at 25(OH)D between 25 and 30?ng/ml. Vitamin D3 supplementation increased serum 25(OH)D and decreased PTH. Change in PTH correlated positively with baseline serum 25(OH)D. From the regression analyses, baseline serum 25(OH)D above 28?ng/ml corresponded to the threshold level without reduction in PTH after vitamin D3 supplementation. In multivariate regression analyses, age but not calcium intake was a significant determinant of PTH. We concluded that a serum 25(OH)D level of 28?ng/ml was identified as a threshold for vitamin D insufficiency necessary to stabilize PTH to optimal levels. 相似文献
4.
James A. Crowell Jr. Cary W. Cooper Svein U. Toverud Agna Boass 《Calcified tissue international》1984,36(1):320-326
Summary Studies presented here were designed to investigate further the basis for an impaired cAMP response to parathyroid hormone
(PTH) in osteoblastlike calvarial bone cells isolated from vitamin D-deficient rat pups. The goal was to perturb Ca, PTH,
and vitamin Din vivo in order to see which factors might be responsible for the impairedin vitro bone cell cAMP response. Pups either were parathyroidectomized (PTX) 3–5 days, implanted with osmotic minipumps delivering
high doses of PTH, given repeated, high doses of 1,25(OH)2D3, or were D-deficient (-D, i.e., born and suckled by D-deficient mothers). Osteoblastlike bone cells, isolated by sequential
enzyme digestion and centrifugation, were exposed to PTH for 5 min in the presence of a phosphodiesterase inhibitor. In bone
cells isolated from -D rat pups, both basal and PTH-induced cAMP accumulation were significantly lower than in +D bone cells.
Earlier, we had shown that two daily injections of -D pups with 50 ng 1,25(OH)2D3 restores this reduced bone cAMP response of -D pups toward normal. In the present study, neither basal nor PTH-induced bone
cell cAMP accumulation was affected by subjecting D-replete pups to PTX, PTH infusion, or repeated high doses of 1,25(OH)2D3 despite the fact that each treatment markedly changed serum Ca or serum immunoreactive PTH. The results indicate that the
impaired bone cell cAMP response seen in -D pups is not a direct result of chronic hypocalcemia and that the “heterologous
desensitization” seenin vitro with added 1,25(OH)2D3 could not be duplicated byin vivo treatment of +D pups with supraphysiologic doses of 1,25(OH)2D3. Finally the lack of alteration in the bone cell cAMP response to PTHin vitro after chronic PTH infusionin vivo fails to support the notion that the impaired response in -D bone cells can be explained entirely by “homologous desensitization”
induced by high circulating levels of PTH in the hypocalcemic, -D rat pup. 相似文献
5.
Background
Vitamin D deficiency is common with bariatric surgery, and few prospective studies comparing different surgical procedures have evaluated appropriate vitamin D supplementation levels. Therefore, vitamin D3 and calcium supplementation were evaluated following gastric bypass and sleeve gastrectomy.Methods
Women consumed 2,000 international units (IU) of vitamin D3 and 1,500 mg calcium citrate daily for 3 months following gastric bypass (n?=?11) and sleeve gastrectomy (n?=?12). Height, weight, body mass index (BMI), serum 25-hydroxyvitamin D [25(OH)D], and serum PTH concentrations were measured preoperatively and at 3 months. Wilcoxon signed rank analyses compared body weight parameters, serum 25(OH)D and PTH concentrations, and dietary intakes of vitamin D and calcium preoperatively and at 3 months. Vitamin D deficiency was defined as a serum 25(OH)D concentration <20 ng/mL (50 nmol/L).Results
Vitamin D deficiency decreased from 60.6 % preoperatively to 26.1 % after 3 months (P?0.005). Serum 25(OH)D concentrations increased an average of 8 ng/mL (P?0.001), and PTH concentrations decreased an average of 9 ng/L, although reductions were not significant. Overall, the response to supplementation following gastric bypass and sleeve gastrectomy did not differ.Conclusions
Reduced food intake increased the risk of vitamin D deficiency following bariatric surgery. However, daily supplementation with 2,000 IU of vitamin D3 and 1,500 mg calcium citrate significantly increased 25(OH)D concentrations and reduced the percent of women who were vitamin D deficient. Although serum 25(OH)D concentrations did not reach levels associated with detrimental health effects, several women remained vitamin D deficient and more aggressive supplementation may be indicated. 相似文献6.
J. W. Nieves F. Cosman E. Grubert B. Ambrose S. H. Ralston R. Lindsay 《Calcified tissue international》2012,91(5):316-324
Black women have lower serum 25-hydroxyvitamin D (25[OH]D) levels and higher parathyroid hormone (PTH) levels than white peers but lower bone turnover, suggesting skeletal resistance to PTH. Our objective was to determine if vitamin D supplementation (1,000?IU/day) would prevent bone loss and whether vitamin D receptor (VDR) polymorphisms modify the response. We performed a 2-year randomized, controlled, double-blind study of 1,000?IU vitamin D3 vs. placebo in postmenopausal black women with serum 25(OH)D levels <20?ng/mL (n?=?103). Measurements of 25(OH)D, PTH, and bone turnover were evaluated at baseline and 3, 6, 12, 18, and 24?months. DNA was extracted from peripheral blood leukocytes, and genotyping was conducted using standard techniques. Spine and hip bone mineral density (BMD) was measured at baseline and every 6?months. Serum 25(OH)D increased 11?ng/mL with vitamin D supplementation (p?<?0.001), with no change in the placebo group. Vitamin D supplementation produced a significant decline in PTH at 3?months only, with no differences in bone turnover between placebo and vitamin D at any time point. Two-year changes in BMD were not significantly different between placebo- and vitamin D-treated black women at any skeletal site. Despite similar elevations in 25(OH)D, femoral neck BMD was only responsive to vitamin D supplementation in FF subjects (n?=?47), not Ff/ff subjects (n?=?31). Vitamin D supplementation does not appear to influence bone loss in black women. However, in the FF polymorphism of the VDR gene group, vitamin D supplementation may retard the higher rate of bone loss. 相似文献
7.
The effect of a short course of calcium and vitamin d on bone turnover in older women 总被引:5,自引:0,他引:5
K. M. Prestwood MD A. M. Pannullo A. M. Kenny C. C. Pilbeam L. G. Raisz 《Osteoporosis international》1996,6(4):314-319
Calcium and vitamin D (1200 mg/day + 800 IU) has been shown to reduce hip fracture incidence in older women living in long-term care facilities who had borderline low vitamin D levels. We examined the effect of a short course of calcium and vitamin D on biochemical markers of bone turnover in older community-living women. Twelve community-living women (mean age 75 years) in good general health, without diseases or on medications known to affect bone, were entered into the study. All women were treated with calcium citrate (1500 mg/day of elemental calcium) and vitamin D3 (1000 IU/day) (Ca + D) for 6 weeks. Biochemical markers of bone turnover were measured in serum and urine collected at baseline (two samples), 5 and 6 weeks on Ca + D, and 5 and 6 weeks after termination of Ca + D. Markers of bone formation were osteocalcin, bone alkaline phosphatase and type I procollagen peptide. Markers of bone resorption were urinary hydroxyproline, free pyridinoline and deoxypyridinoline crosslinks, and N-telopeptides of type I collagen. Parathyroid hormone (PTH) and 25-hydroxyvitamin D were also measured at baseline, 6 weeks on treatment and 6 weeks after termination of treatment. All markers of bone resorption decreased on Ca + D and returned to baseline after termination of Ca + D (p<0.05). Markers of bone formation did not change with Ca + D treatment. PTH decreased on Ca + D and returned to baseline after treatment, and 25-hydroxyvitamin D increased with treatment and remained elevated 6 weeks after the end of treatment. We conclude that Ca + D reduces bone resorption in older women, possibly by suppressing PTH levels. 相似文献
8.
A. Shiraishi S. Higashi H. Ohkawa N. Kubodera T. Hirasawa I. Ezawa K. Ikeda E. Ogata 《Calcified tissue international》1999,65(4):311-316
Although alfacalcidol is widely used in the treatment of osteoporosis, its mechanism of action in bone is not fully understood.
Alfacalcidol stimulates intestinal calcium (Ca) absorption, increases urinary Ca excretion and serum Ca levels, and suppresses
parathyroid hormone (PTH) secretion. It remains to be clarified, especially under vitamin D-replete conditions, whether alfacalcidol
exerts skeletal effects solely via these Ca-related effects, whether the resultant suppression of PTH is a prerequisite for
the skeletal actions of alfacalcidol, and, by inference, whether alfacalcidol has an advantage over vitamin D in the treatment
of osteoporosis. To address these issues, we (1) compared the effects of alfacalcidol p.o. (0.025–0.1 μg/kg BW) vis-à-vis
vitamin D3 (50–400 μg/kg BW) on bone loss in 8-month-old, ovariectomized (OVX) rats as a function of their Ca-related effects, and (2)
examined whether the skeletal effects of alfacalcidol occur independently of suppression of PTH, using parathyroidectomized
(PTX) rats continuously infused with hPTH(1–34). The results indicate that (1) in OVX rats, alfacalcidol increases BMD and
bone strength more effectively than vitamin D3 at given urinary and serum Ca levels: larger doses of vitamin D3 are required to produce a similar BMD-increasing effect, in the face of hypercalcemia and compromised bone quality; (2) at
doses that maintain serum Ca below 10 mg/dl, alfacalcidol suppresses urinary deoxypyridinoline excretion more effectively
than vitamin D3; and (3) alfacalcidol is capable of increasing bone mass in PTX rats with continuous infusion of PTH, and therefore acts
independently of PTH levels. It is suggested that alfacalcidol exerts bone-protective effects independently of its Ca-related
effects, and is in this respect superior to vitamin D3, and that the skeletal actions of alfacalcidol take place, at least in part, independently of suppression of PTH. Together,
these results provide a rationale for the clinical utility of alfacalcidol and its advantage over vitamin D3 in the treatment of osteoporosis. 相似文献
9.
Jacob J. Vandersteenhoven Frank A. DeLustro Norman H. Bell M.D. Russell T. Turner 《Calcified tissue international》1988,42(1):39-45
Summary Experimental heterotopic bone formation was produced by subcutaneous implants of demineralized allogeneic bone matrix (DABM)
in vitamin D-deficient (−D) animals that were either not treated or given vitamin D3 (+D) or 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) to determine the role of vitamin D and its most active metabolite in osteoinduction and implant remodeling. Histologically,
implants in both +D and −D groups caused a similar acute inflammatory response, formation of a fibrous capsule, and chondrogenesis
by 1 to 2 weeks after implantation. However, by 3 weeks after implantation implants in the −D animals had formed less bone
matrix, had developed a defect in matrix mineralization, had reduced bone forming and bone resorbing surfaces, and had altered
bone architecture resulting from defective bone remodeling. The altered histology in −D animals was not corrected by 10 weeks
after implantation. Treatment of vitamin D-deficient rats with 1,25(OH)2D3, 65 pmol/day for 3 weeks, corrected both the defect in mineralization and the abnormal histology. The results indicate that
(1) vitamin D deficiency does not alter either the timing or the sequence of histologic events associated with osteoinduction
but dramatically reduces the magnitude of the response, (2) vitamin D deficiency not only impairs mineralization but also
reduces bone formation and resorption, and (3) 1,25(OH)2D3 mimics all of the actions of vitamin D with regard to correcting the abnormal osteoinductive response and bone histomorphometry. 相似文献
10.
Summary Weanling rats were given a vitamin D-deficient diet containing 1.4% calcium and 1.0% phosphorus. After 4 weeks these deficient
animals were injected for 7 days with selected doses of one of the following vitamin D metabolites: 25(OH)D3, 1,25(OH)2D3, 24,25(OH)2D3, 25,26(OH)2D3 or the ethanol vehicle. A vitamin D-replete group was placed on the same diet but injected with 50 IU of vitamin D3 once a week for the entire 5-week period. By the use of a modified Ussing chamber [1], the measurements of calcium fluxes
into and from the rat calvaria were possible. These data enabled the apparent mineral solubilities to be derived.
After 5 weeks on this diet the vitamin D-deficient rats had low levels of serum calcium (1.41 mM) and decreased mineral solubility
when compared to the vitamin D-replete group. The apparent solubility of the bone mineral increased toward the vitamin D-replete
level in calvaria from vitamin D metabolite-treated rats. However, these changes did not directly reflect the alterations
in the level of serum calcium. At any given dose level, 1,25(OH)2D3 was the most effective metabolite in increasing serum calcium. In fact, the high dose (250 pmoles/day) was hypercalcemic.
Next in effectiveness was 25(OH)D3. These two metabolites were equally effective in increasing mineral solubility. At a 10 times higher dose, the 24,25(OH)2D3 metabolite was able to normalize serum calcium and improve but not normalize mineral solubility. At the high dose (260 pmoles/day),
the 25,26(OH)2D3 metabolite caused no effect on mineral solubility and minimal increases in serum calcium. 相似文献
11.
S. C. Miller B. P. Halloran H. F. DeLuca S. Yamada H. Takayama W. S. S. Jee 《Calcified tissue international》1981,33(1):489-497
Summary To test the importance of 24-hydroxylation of vitamin D3 on bone mineralization, rat pups born to vitamin D-deficient females were given either 25-hydroxyvitamin D3 or 24,24-difluoro-25-hydroxyvitamin D3 for 16 days beginning at the time of weaning. Following such treatment analysis of blood samples revealed no detectable 24R,25-(OH)2D3 and 1,25-(OH)2D3 in the rats given the difluoro compound while revealing the expected 24,24-difluoro-25-hydroxyvitamin D3 and 24,24-difluoro-1,25-dihydroxyvitamin D3. The rats given 25-hydroxyvitamin D3 had the expected levels of 25-hydroxyvitamin D3, 24,25-dihydroxyvitamin D3, and 1,25-dihydroxyvitamin D3. Following sacrifice at day 17, postweaning bone mineralization and modeling were studied in long bones using histological
methods. Bones taken from vitamin D-deficient rats at the beginning and end of the experimental period had lesions typical
of rickets. These included wide growth plates, excessive amounts of osteoid, and metaphyseal fibrosis. Following treatment
with either 25-hydroxyvitamin D3 or 24,24-difluoro-25-hydroxyvitamin D3, bone mineralization returned to normal. Growth plate widths and the amount of osteoid on bone surfaces were both substantially
reduced and to a similar degree in both treatment groups. Normal cartilage core formation and trabecularization of the metaphyseal
primary spongiosa were also restored to a similar degree in both groups. In effect, no difference was observed in any bone
parameter studied between the 25-hydroxyvitamin D3- and the 24,24-difluoro-25-hydroxyvitamin D3-treated animals. These results provide strong evidence that 24-hydroxylation of the vitamin D molecule plays little or no
role in the modeling and mineralization of bone. 相似文献
12.
Effect of 1α-hydroxyvitamin D3 and egg-shell calcium on bone metabolism in ovariectomized osteoporotic model rats 总被引:1,自引:0,他引:1
Egg-shell calcium (Ca) is one of the effective Ca sources for bone metabolism. In the present study, we investigated whether
egg-shell Ca had similar effects compared with calcium carbonate (CaCO3) when vitamin D3 (1α(OH)D3) treatment was given to an osteopo-rotic rat model. In both 1α(OH)D3-supplemented and -unsupplemented rats, the bone mineral density (BMD) of the lumber spine in the vitamin-supplemented group
increased significantly compared with the unsupplemented group. In a Ca balance study, there were also significant differences
in intestinal Ca absorption, urinary Ca and fecal Ca between the vitamin-supplemented and -unsupplemented groups. These results
show that egg-shell Ca could have similar effects to CaCO3 on bone metabolism. In contrast with CaCO3, vitamin D3 supplementation did not significantly increase serum Ca levels in the egg-shell Ca group; however, the mechanism of Ca absorption
is still unclear. Our results suggest that egg-shell Ca may be an effective nutrient in Ca metabolism for people treated with
vitamin D3.
Received: January 6, 2000 / Accepted: July 31, 2000 相似文献
13.
Association Between Single Gene Polymorphisms and Bone Biomarkers and Response to Calcium and Vitamin D Supplementation in Young Adults Undergoing Military Training
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Erin Gaffney‐Stomberg Laura J Lutz Anna Shcherbina Darrell O Ricke Martha Petrovick Thomas L Cropper Sonya J Cable James P McClung 《Journal of bone and mineral research》2017,32(3):498-507
Initial military training (IMT) is associated with increased stress fracture risk. In prior studies, supplemental calcium (Ca) and vitamin D provided daily throughout IMT reduced stress fracture incidence, suppressed parathyroid hormone (PTH), and improved measures of bone health compared with placebo. Data were analyzed from a randomized, double‐blind, placebo‐controlled trial to determine whether single‐nucleotide polymorphisms (SNPs) in Ca and vitamin D–related genes were associated with circulating biomarkers of bone metabolism in young adults entering IMT, and whether responses to Ca and vitamin D supplementation were modulated by genotype. Associations between SNPs, including vitamin D receptor (VDR), vitamin D binding protein (DBP), and 1‐alpha‐hydroxylase (CYP27B1), and circulating biomarkers were measured in fasting blood samples from volunteers (n = 748) starting IMT. Volunteers were block randomized by race and sex to receive Ca (2000 mg) and vitamin D (1000 IU) or placebo daily throughout Army or Air Force IMT (7 to 9 weeks). Total Ca and vitamin D intakes were calculated as the sum of supplemental intake based on intervention compliance and dietary intake. Relationships between SNPs, Ca, and vitamin D intake tertile and change in biomarkers were evaluated in trial completers (n = 391). At baseline, the minor allele of a DBP SNP (rs7041) was positively associated with both 25OHD (B = 4.46, p = 1.97E‐10) and 1,25(OH)2D3 (B = 9.63, p < 0.001). Combined genetic risk score (GRS) for this SNP and a second SNP in the VDR gene (rs1544410) was inversely associated with baseline 25OHD (r = –0.28, p < 0.001) and response to Ca and vitamin D intake differed by GRS (p < 0.05). In addition, presence of the minor allele of a second VDR SNP (rs2228570) was associated with lower P1NP (B = –4.83, p = 0.04) and osteocalcin (B = –0.59, p = 0.03). These data suggest that VDR and DBP SNPs are associated with 25OHD status and bone turnover and those with the highest GRS require the greatest vitamin D intake to improve 25OHD during IMT. © 2016 American Society for Bone and Mineral Research. 相似文献
14.
Dr. M. Gunness-Hey I. Gera J. Fonseca L. G. Raisz J. M. Hock 《Calcified tissue international》1988,43(5):284-288
Summary Parathyroid hormone (PTH) alone is known to increase bone mass, but clinical studies of osteoporotic men suggest that when
1,25 dihydroxyvitamin D3 (1,25(OH)2D3) is given in combination with PTH, the effect on bone growth is enhanced. To determine if 1,25(OH)2D3 alone would stimulate bone growth, young male rats were given daily subcutaneous injections of either vehicle or 2.5, 5,
10, or 20 ng 1,25(OH)2D3 per 100 g body weight for 30 days. To determine if 1,25(OH)2D3 would augment the PTH anabolic response, rats were given daily subcutaneous injections of either vehicle for 12 days; or
4 μg/100 g hPTH alone or in combination with 5 ng/100 g 1,25(OH)2D3; or 8 μg/100 g hPTH alone or in combination with 5 ng/100 g 1,25(OH)2D3. Calcium (Ca), dry weight (DW), and hydroxyproline (Hyp) of the distal femur; the rate of mineralization in the metaphysis
of the proximal tibia; and serum calcium and phosphate were measured. Low normocalcemic doses of 1,25(OH)2D3 did not significantly stimulate bone growth. 1,25(OH)2D3 did not augment the PTH-stimulated anabolic effect in young male rats. Low doses (2.5 and 5 ng) of 1,25(OH)2D3 were not hypercalcemic, and there was no increase in total bone calcium or dry weight although the 5 ng dose increased trabecular
bone calcium. 1,25(OH)2D3 at 10 and 20 ng increased trabecular bone DW and Hyp, but mineralization was impaired and rats were hypercalcemic. 1,25(OH)2D3 in combination with PTH did not augment the PTH stimulation of bone growth as trabecular and cortical bone Ca, DW, and HYP
were not increased in rats given both hPTH and 1,25(OH)2D3 compared with values for rats treated with hPTH alone. 相似文献
15.
Heli T Viljakainen Milja Väisänen Virpi Kemi Toni Rikkonen Heikki Kröger E Kalevi A Laitinen Hannu Rita Christel Lamberg‐Allardt 《Journal of bone and mineral research》2009,24(2):346-352
Vitamin D is suggested to have a role in the coupling of bone resorption and formation. Compared with women, men are believed to have more stable bone remodeling, and thus, are considered less susceptible to the seasonal variation of calcitropic hormones. We examined whether seasonal variation exists in calcitropic hormones, bone remodeling markers, and BMD in healthy men. Furthermore, we determined which vitamin D intake is required to prevent this variation. Subjects (N = 48) were healthy white men 21–49 yr of age from the Helsinki area with a mean habitual dietary intake of vitamin D of 6.6 ± 5.1 (SD) μg/d. This was a 6‐mo double‐blinded vitamin D intervention study, in which subjects were allocated to three groups of 20 μg (800 IU), 10 μg (400 IU), or placebo. Fasting blood samplings were collected six times for analyses of serum (S‐)25(OH)D, iPTH, bone‐specific alkaline phosphatase (BALP), and TRACP. Radial volumetric BMD (vBMD) was measured at the beginning and end of the study with pQCT. Wintertime variation was noted in S‐25(OH)D, S‐PTH, and S‐TRACP (p < 0.001, p = 0.012, and p < 0.05, respectively) but not in S‐BALP or vBMD in the placebo group. Supplementation inhibited the winter elevation of PTH (p = 0.035), decreased the S‐BALP concentration (p < 0.05), but benefited cortical BMD (p = 0.09) only slightly. Healthy men are exposed to wintertime decrease in vitamin D status that impacts PTH concentration. Vitamin D supplementation improved vitamin D status and inhibited the winter elevation of PTH and also decreased BALP concentration. The ratio of TRACP to BALP shows the coupling of bone remodeling in a robust way. A stable ratio was observed among those retaining a stable PTH throughout the study. A daily intake of vitamin D in the range of 17.5–20 μg (700–800 IU) seems to be required to prevent winter seasonal increases in PTH and maintain stable bone turnover in young, healthy white men. 相似文献
16.
Normal intestinal calcium (Ca) absorption is an essential feature of bone homeostasis. As with many other organ systems,
intestinal Ca absorption declines with aging, and this is one pathological factor that has been identified as a cause of senile
osteoporosis in the elderly. This abnormality leads to secondary hyperparathyroidism, which is characterized by high serum
parathyroid hormone (PTH) and an increase in bone resorption. Secondary hyperparathyroidism due to poor intestinal Ca absorption
has been implicated not only in senile osteoporosis but also in age-related bone loss. Accordingly, in population-based studies,
there is a gradual increase in serum PTH from about 20 years of age onward, which constitutes a maximum increase at 80 years
of age of 50% of the basal value seen at 30 years of age. The cause of the increase in PTH is thought to be partly due to
impaired intestinal Ca absorption that is associated with aging, a cause that is not entirely clear but at least in some instances
is related to some form of vitamin D deficiency. There are three types of vitamin D deficiency: (1) primary vitamin D deficiency,
which is due to a deficiency of vitamin D, the parent compound; (2) a deficiency of 1,25(OH)2D3 resulting from decreased renal production of 1,25(OH)2D3; and (3) resistance to 1,25(OH)2D3 action owing to decreased responsiveness to 1,25(OH)2D3 of target tissues. The cause for the resistance to 1,25(OH)2D3 could be related to the finding that the vitamin D receptor level in the intestine tends to decrease with age. All three
types of deficiencies can occur with aging, and each has been implicated as a potential cause of intestinal Ca malabsorption,
secondary hyperparathyroidism, and senile osteoporosis. There are two forms of vitamin D replacement therapies: plain vitamin
D therapy and active vitamin D analog (or D-hormone) therapy. Primary vitamin D deficiency can be corrected by vitamin supplements
of 1000 U a day of plain vitamin D whereas 1,25(OH)2D3 deficiency/resistance requires active vitamin D analog therapy [1,25(OH)2D3 or 1α(OH)D3] to correct the high serum PTH and the Ca malabsorption. In addition, in the elderly, there are patients with decreased intestinal
Ca absorption but with apparently normal vitamin D metabolism. Although the cause of poor intestinal Ca absorption in these
patients is unclear, these patients, as well as all other patients with secondary hyperparathyroidism (not due to decreased
renal function), show a decrease in serum PTH and an increase in Ca absorption in response to therapy with 1,25(OH)2D3 or 1α(OH)D3. In short, it is clear that some form of vitamin D therapy, either plain vitamin D or 1,25(OH)2D3 or 1α(OH)D3, can be used to correct all types of age-dependent impairments in intestinal Ca absorption and secondary hyperparathyroidism
during aging. However, from a clinical standpoint, it is important to recognize the type of vitamin D deficiency in patients
with senile osteoporosis so that primary vitamin D deficiency can be appropriately treated with plain vitamin D therapy, whereas
1,25(OH)2D3 deficiency/resistance will be properly treated with 1,25(OH)2D3 or 1α(OH)D3 therapy. With respect to postmenopausal osteoporosis, there is strong evidence that active vitamin D analogs (but not plain
vitamin D) may have bone-sparing actions. However, these effects appear to be results of their pharmacologic actions on bone
formation and resorption rather than through replenishing a deficiency. 相似文献
17.
Albert Fournier Roxana Oprisiu Carine Hottelart Paule Hardy Yverneau Abderahmane Ghazali Ahcène Atik Hafed Hedri Said Said Anne Sechet Mireille Rasolombololona Oussama Abighanem Ayman Sarraj Najeh El Esper Philippe Moriniere Bernard Boudailliez Pierre-François Westeel Jean-Michel Achard & André Pruna 《Artificial organs》1998,22(7):530-557
Abstract: This article reviews the clinical, biological, radiological, and pathological procedures and their respective indications for the practical diagnosis of the following various histological patterns of renal osteodystrophy: osteitis fibrosa due to parathyroid hormone (PTH) hypersecretion; osteomalacia or rickets due to native vitamin D deficiency and/or aluminum overload; and adynamic bone disease (ABD) due to aluminum overload and/or PTH secretion oversuppression. Our advice regarding bone biopsy is to restrict it to patients with symptoms and hypercalcemia, especially those who have been previously exposed to aluminum. In other cases, we propose relying merely on the determination of the plasma concentrations of calcium, protide, phosphate, bicarbonate, intact PTH, aluminum, 25(OH)D3, and alkaline phosphatase (total and bony if hepatic disease is associated) to choose the appropriate treatment. Because of the danger of the desferrioxamine treatment necessary to chelate and remove aluminum, the suspicion of aluminic bone disease (osteomalacia or ABD) will always be confirmed by a bone biopsy. In the case of nonaluminic osteomalacia, correction of the vitamin D deficiency by native vitamin D or 25(OH)D3, and of the calcium deficiency and acidosis by alkaline salts of calcium and if necessary sodium bicarbonate are sufficient to cure the disease. In the case of nonaluminic ABD, the stimulation of PTH secretion by the discontinuation of 1α hydroxylated vitamin D and the induction of a negative calcium balance during dialysis by decreasing the calcium concentration in the dialysate will allow an increase of the CaCO3 dose to correct for hyperphosphatemia without inducing hypercalcemia. For hyperparathyroidism, i.e., plasma intact PTH levels greater than two- or four-fold the upper limit of normal levels (according to the absence or presence of previous aluminum exposure), the treatment will consist in increasing the CaCO3 dose to correct for hyperphosphatemia together with a decrease of the calcium concentration in the dialysate if the dose of CaCO3 is so high that it induces hypercalcemia. When the hyperphosphatemia has been corrected and there is still a low or normal corrected plasma calcium level, 1α(OH)D3 in an oral bolus 2 or 3 times a week should be given at the minimal dose of 1 μg. When the PTH level stays above 400 pg while hypercalcemia occurs and hyperphosphatemia persists, surgical subtotal parathyroidectomy is recommended or the injection of calcitriol into the big nodular hyperplastic parathyroid glands under sonography control in high surgical risk patients. Special recommendations are given for children. 相似文献
18.
R. Przybelski S. Agrawal D. Krueger J. A. Engelke F. Walbrun N. Binkley 《Osteoporosis international》2008,19(11):1621-1628
Summary This prospective study finds that ergocalciferol 50,000 IU three times weekly for four weeks effectively and safely corrects
vitamin D inadequacy in nursing home residents.
Introduction Low vitamin D status is common among nursing home residents and contributes to bone loss, falls and fractures. The objective
of this study was to evaluate the efficacy and safety of short course, high dose, oral vitamin D2 (ergocalciferol) treatment.
Methods This prospective study included 63 nursing home residents. The 25 with low vitamin D status (serum 25(OH)D ≤ 25 ng/ml) received
oral ergocalciferol 50,000 IU three times weekly for four weeks; the others received no change to their routine care. Serum
total 25(OH)D, 25(OH)D2, 25(OH)D3, calcium, parathyroid hormone (PTH), bone turnover markers and neuro-cognitive assessments were obtained at baseline and
four weeks.
Results Mean total 25(OH)D concentration increased (p < 0.0001) from 17.3 to 63.8 ng/ml in the treated group and remained unchanged
in the comparison group. Serum 25(OH)D3 remained stable in the comparison group, but declined (p < 0.0001) with D2 treatment from 15.4 to 9.1 ng/ml. Serum PTH trended down in the treatment group (p = 0.06). No treatment-induced improvement
in ambulation, cognition or behavior was observed. No hypercalcemia or other adverse effects were observed with ergocalciferol
treatment.
Conclusion Four weeks of oral vitamin D2 supplementation effectively and safely normalizes serum 25(OH)D in nursing home residents. 相似文献
19.
R. M. Francis 《Calcified tissue international》1997,60(1):111-114
There is a decline in serum 25 hydroxyvitamin D (25OHD), 1,25 dihydroxyvitamin D (1,25(OH)2D), and calcium absorption with advancing age, which may lead to secondary hyperparathyroidism and bone loss. Studies show
a relationship between serum 25OHD and bone density in older men and women, with an inverse correlation between bone density
and parathyroid hormone (PTH). Vitamin D supplementation in this age group improves calcium absorption, suppresses PTH, and
decreases bone loss. Vitamin D many also reduce the incidence of hip and other nonvertebral fractures, particularly in the
frail elderly who are likely to have vitamin D deficiency. Patients with established vertebral osteoporosis have lower calcium
absorption than age-matched control subjects, possibly due to reduced serum 1,25(OH)2D or to relative resistance to the action of vitamin D on the bowel. Malabsorption of calcium in women with vertebral crush
fractures does not usually respond to treatment with physiological doses of vitamin D, but can be corrected by pharmacological
doses of vitamin D or by low doses of calcitriol or alfacalcidol. In a recent randomized, controlled study in 46 elderly women
with radiological evidence of vertebral osteoporosis, alfacalcidol 0.25 μg twice daily improved calcium absorption, decreased
serum PTH, and reduced alkaline phosphatase, whereas vitamin D2 500–1000 IU daily had no effect over the 6-month study period. Studies of the effect of the vitamin D metabolites in the
management of elderly women with established vertebral osteoporosis have yielded conflicting results, but suggest that alfacalcidol
and calcitriol may decrease spinal bone loss and reduce the incidence of vertebral fractures. Although vitamin D supplementation
decreases bone loss and fracture risk in the frail elderly, vitamin D metabolites may prove more useful in the treatment of
elderly women with vertebral osteoporosis. 相似文献
20.
Russell T. Turner Norman H. Bell David J. Baylink 《Calcified tissue international》1983,35(1):438-442
Summary To determine the effects of 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] on the renal metabolism of 25-hydroxyvitamin D3 [25(OH)D3], the influence of 1,25(OH)2D3 and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] was compared in vitamin D-deficient rats. Serum calcium (Ca), serum immunoreactive parathyroid hormone (iPTH) and the specific
activities (SA) of renal 25(OH)D3: 24-hydroxylase (24-hydroxylase) and 25(OH)D3: 1α-hydroxylase (1-hydroxylase) were measured. In vitamin D-deficient rats, mean serum Ca was low, serum iPTH was increased,
renal 1-hydroxylase was increased, and renal 24-hydroxylase was below the limit of detection. Treatment with either 1,25(OH)2D3 or 24,25(OH)2D3, 50 ng/d for 2 days, significantly increased mean serum Ca but did not change serum iPTH, renal 1-hydroxylase SA, or renal
24-hydroxylase SA. 1,25(OH)2D3, 50 ng/d for 7 days, returned serum Ca and iPTH to normal, lowered renal 1-hydroxylase SA, and induced renal 24-hydroxylase
activity. In contrast, 24,25(OH)2D3, 50 ng/d for 7 days, similarly lowered renal 1-hydroxylase SA but did not induce renal 24-hydroxylase activity. Thyroparathyroidectomy
of vitamin D-deficient rats resulted in a rapid decline in 1-hydroxylase SA. The results indicate that in vitamin D-deficient
rats a) 1,25(OH)2D3 reduces renal 1-hydroxylase SA and increases renal 24-hydroxylase SA and b) 24,25(OH)2D3 reduces renal 1-hydroxylase SA and does not alter renal 24-hydroxylase SA. Inhibition of renal 1-hydroxylase by the two metabolites
is apparently mediated through changes in serum Ca and circulating iPTH, whereas stimulation by 1,25(OH)2D3 of renal 24-hydroxylase activity is direct. 相似文献