Influence of Long-Term Oral 1,25-Dihydroxyvitamin D in Childhood Renal Osteodystrophy1

2015 ◽  
pp. 55-71 ◽  
Author(s):  
Russell W. Chesney ◽  
A. Hamstra ◽  
Diane K. Jax ◽  
Richard B. Mazess ◽  
Hector F. DeLuca
Keyword(s):  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

Long-term intracaval calcium infusion therapy in end-organ resistance to 1,25-dihydroxyvitamin D

1987 ◽  
Vol 83 (5) ◽  
pp. 984-990 ◽  
Author(s):  
Yosef Weisman ◽  
Itay Bab ◽  
Dan Gazit ◽  
Zvi Spirer ◽  
Michael Jaffe ◽  
...  
Keyword(s):  
Infusion Therapy ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Calcium Infusion

scholarly journals Effect of 1,25-dihydroxyvitamin D3 on spontaneous calcium responses in rat dental epithelial SF2 cells revealed by long-term imaging

2016 ◽  
Vol 37 (6) ◽  
pp. 329-334
Author(s):  
Kaori MURATA ◽  
Ayumi TAKAHASHI ◽  
Takao MORITA ◽  
Akihiro NEZU ◽  
Satoshi FUKUMOTO ◽  
...  
Keyword(s):  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

Long-term vitamin D deficiency promotes renal fibrosis and functional impairment in middle-aged male mice

2020 ◽  
pp. 1-10
Author(s):  
Zhi-Hui Zhang ◽  
Biao Luo ◽  
Shen Xu ◽  
Zhi-Cheng Zhang ◽  
Wei-Yang Xing ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Functional Impairment ◽  
Renal Fibrosis ◽  
Male Mice ◽  
Middle Aged ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Middle Aged Male

Abstract Renal fibrosis is common especially in the elderly population. Recently, we found that vitamin D deficiency caused prostatic hyperplasia. This study aimed to investigate whether vitamin D deficiency promotes renal fibrosis and functional impairment. All mice except controls were fed with vitamin D-deficient (VDD) diets, beginning from their early life. The absolute and relative kidney weights on postnatal week 20 were decreased in VDD diet-fed male pups but not in female pups. A mild pathological damage was observed in VDD diet-fed male pups but not in females. Further analysis showed that VDD-induced pathological damage was aggravated, accompanied by renal dysfunction in 40-week-old male pups. An obvious collagen deposition was observed in VDD diet-fed 40-week-old male pups. Moreover, renal α-smooth muscle actin (α-SMA), a marker of epithelial–mesenchymal transition (EMT), and Tgf-β mRNA were up-regulated. The in vitro experiment showed that 1,25-dihydroxyvitamin D3 alleviated transforming growth factor-β1 (TGF-β1)-mediated down-regulation of E-cadherin and inhibited TGF-β1-evoked up-regulation of N-cadherin, vimentin and α-SMA in renal epithelial HK-2 cells. Moreover, 1,25-dihydroxyvitamin D3 suppressed TGF-β1-evoked Smad2/3 phosphorylation in HK-2 cells. These results provide experimental evidence that long-term vitamin D deficiency promotes renal fibrosis and functional impairment, at least partially, through aggravating TGF-β/Smad2/3-mediated EMT in middle-aged male mice.

Calcium homeostasis in chronic streptozotocin-induced diabetes mellitus in the rat

1982 ◽  
Vol 242 (6) ◽  
pp. E451-E456 ◽  
Author(s):  
S. Hough ◽  
J. E. Russell ◽  
S. L. Teitelbaum ◽  
L. V. Avioli
Keyword(s):  
Insulin Therapy ◽  
Calcium Homeostasis ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Calcium Balance ◽  
Short Term ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Streptozotocin Induced Diabetes

Calcium homeostasis was studied in freely fed control, streptozotocin diabetic, long-term and short-term insulin-treated diabetic rats 7 wk after the induction of diabetes. In contrast to the short-term (5-12 day) diabetic rat model, intestinal absorption of calcium was markedly enhanced in chronically insulin-deficient animals. Moreover, conventional balance studies showed that these animals were in positive calcium balance despite severe hypercalciuria. Intestinal hyperabsorption of calcium in long-standing diabetic rats occurred despite low levels of circulating 1,25-dihydroxyvitamin D and hypercorticosteronism and was attended by hypercalcemia and suppression of both plasma parathyroid hormone (PTH) and urinary cyclic 3',5'-AMP (cAMP). Long-term insulin replacement completely normalized the intestinal hyperabsorption of calcium, corrected the plasma calcium, and significantly increased circulating PTH and urinary cAMP excretion. Insulin therapy also corrected the decreased plasma 1,25-dihydroxyvitamin D observed in untreated diabetic animals. Intestinal hyperabsorption of calcium appeared to be only partially corrected by short-term insulin therapy. The accumulated results reveal decided differences in calcium homeostasis and hormonal response between the rats with long-standing diabetes and those with diabetes of short duration.

scholarly journals Long-term nocturnal calcium infusions can cure rickets and promote normal mineralization in hereditary resistance to 1,25-dihydroxyvitamin D.

1986 ◽  
Vol 77 (5) ◽  
pp. 1661-1667 ◽  
Author(s):  
S Balsan ◽  
M Garabédian ◽  
M Larchet ◽  
A M Gorski ◽  
G Cournot ◽  
...  
Keyword(s):  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

Hereditary 1,25-dihydroxyvitamin D-resistant rickets (HVDRR): clinical heterogeneity and long-term efficacious management of eight patients from four unrelated Arab families with a loss of function VDR mutation

2018 ◽  
Vol 31 (8) ◽  
pp. 861-868 ◽  
Author(s):  
Muhammad Faiyaz-Ul-Haque ◽  
Waheeb AlDhalaan ◽  
Abdullah AlAshwal ◽  
Bassam S. Bin-Abbas ◽  
Afaf AlSagheir ◽  
...  
Keyword(s):  
Vitamin D ◽  
Target Genes ◽  
Clinical Symptoms ◽  
Active Form ◽  
Loss Of Function ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Vitamin D Resistant Rickets ◽  
Resistant Rickets

Abstract Background: Vitamin D regulates the concentrations of calcium and phosphate in blood and promotes the growth and remodeling of bones. The circulating active form of vitamin D, 1,25-dihydroxyvitamin D, binds to the vitamin D receptor (VDR), which heterodimerizes with the retinoid X receptor to regulate the expression of target genes. Inactivating mutations in the VDR gene cause hereditary vitamin D-resistant rickets (HVDRR), a rare disorder characterized by an early onset of rickets, growth retardation, skeletal deformities, hypocalcemia, hypophosphatemia and secondary hyperparathyroidism, and in some cases alopecia. Methods: We describe eight new HVDRR patients from four unrelated consanguineous families. The VDR gene was sequenced to identify mutations. The management of patients over a period of up to 11 years following the initial diagnosis is assessed. Results: Although all patients exhibit main features of HVDRR and carry the same c.885C>A (p.Y295*) loss of function mutation in the VDR gene, there was heterogeneity of the manifestations of HVDRR-associated phenotypes and developmental milestones. These eight patients were successfully treated over a period of 11 years. All clinical symptoms were improved except alopecia. Conclusions: The study concludes that VDR sequencing and laboratory tests are essential to confirm HVDRR and to assess the effectiveness of the treatment.

Effects of Retinoic Acid and 1,25-Dihydroxyvitamin D3 on IFN-gamma Secretion by Mononuclear Leukocytes from Nulliparous and Postparturient Dairy Cattle

2000 ◽  
Vol 70 (3) ◽  
pp. 92-101 ◽  
Author(s):  
Burim Ametaj ◽  
Brian Nonnecke ◽  
Ronald Horst ◽  
Donald Beitz
Keyword(s):  
Retinoic Acid ◽  
Dairy Cattle ◽  
Dairy Cows ◽  
Dairy Cow ◽  
Pokeweed Mitogen ◽  
Mononuclear Leukocytes ◽  
Combined Effects ◽  
Ifn Gamma ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

Individual and combined effects of several isomers of retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on interferon-gamma (IFN-gamma) secretion by blood mononuclear leukocytes (MNL) from nulliparous and postparturient Holstein cattle were evaluated in vitro. In the first experiment, effects on incubation period (24 to 72 hours) and time of supplementation (0 to 32 hours) with all-trans, 9-cis, 13-cis-, and 9,13-dicis-RAs (0 to 100 nM) on IFN-gamma secretion by pokeweed mitogen (PWM)-stimulated (0 and 10 mug/ml) MNL from nulliparous cattle were evaluated. In the second experiment, MNL from postparturient cows (bled at 0, 2, 4, and 16 days postpartum) were stimulated with PWM (0 and 10 mug/ml) in the presence of RA isomers (9-cis- or 9,13-dicis-RA; 0 to 100 nM), 1,25-(OH)2D3 (0 to 100 nM), or with combinations of these metabolites. The results show that individual isomers of RA had no effect on IFN-gamma secretion by PWM-stimulated MNL from nulliparous or postparturient cows. Furthermore 1,25-dihydroxyvitamin D3 inhibited IFN-gamma secretion by MNL from nulliparous and postparturient dairy cows; however, the degree of inhibition was greater when 9-cis- and 9,13-dicis-RA were also present in the cultures. Finally mononuclear leukocytes from postparturient dairy cows produced substantially less IFN-gamma than did MNL from nulliparous cattle. It is concluded that retinoic acids individually did not affect the capacity of leukocytes from dairy cattle to secrete IFN-gamma. This result is in marked contrast to studies in monogastric species indicating that RAs inhibit IFN-gamma secretion by peripheral blood T cells. Inhibition of IFN-gamma secretion by 1,25-(OH)2D3 was potentiated by 9-cis- and 9,13-di-cis-retinoics acids, suggesting that an excess of dietary vitamins A and D may compromise further the naturally immunosuppressed postparturient dairy cow. Additional research is necessary to determine if the combined effects of these metabolites on IFN-gamma secretion represent an increased susceptibility of the dairy cow to infectious diseases during the periparturient period. Lower secretion of IFN-gamma by MNL from postpartutient dairy cows, relative to nulliparous cattle, suggests that recently-calved cows are naturally immunosuppressed.

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