scholarly journals The effect of disodium ethane-1-hydroxy-1,1-diphosphonate on the metabolism of calcitriol in chicks

1987 ◽  
Vol 243 (1) ◽  
pp. 75-78 ◽  
Author(s):  
C Lidor ◽  
M S Meyer ◽  
R H Wasserman ◽  
S Edelstein
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Intestinal Absorption ◽  
Binding Protein ◽  
Sole Source ◽  
Treated Group ◽  
Response To Treatment ◽  
Vitamin D Metabolism ◽  
Calbindin D28k ◽  
25 Hydroxycholecalciferol

Decreased intestinal absorption of Ca2+ occurs in response to treatment with disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP). The effect is due to decreased 1-hydroxylation of calcidiol (25-hydroxycholecalciferol) in the kidney. In an attempt to establish whether impairment of vitamin D metabolism at steps beyond kidney hydroxylation occurs due to treatment with EHDP, chicks were depleted of vitamin D and were treated with calcitriol (1,25-dihydroxycholecalciferol) as their sole source of the vitamin. The chicks were then divided into two groups, one being treated with EHDP while the second group served as control. Intestinal absorption of Ca2+ in the EHDP-treated group was found to be impaired, along with decreases in concentrations of calbindin D28K (the 28,000-Mr vitamin D-dependent Ca2+-binding protein). When the chicks were dosed with [3H]calcitriol, significantly lower concentrations of the sterol were detected in the duodena of EHDP-treated birds. Measurement of levels of receptors for calcitriol in duodena showed no difference between groups, but levels of calcitriol in sera were considerably lower in the EHDP-treated group along with the elevated biliary and urinary excretion of glucuronidated conjugates. It is therefore concluded that treatment with EHDP results in increased catabolism of calcitriol in addition to the known suppression of the renal production of the hormone.

Vitamin D homeostasis is compromised due to increased urinary excretion of the 25-hydroxycholecalciferol-vitamin D-binding protein complex in the Zucker diabetic fatty rat

2010 ◽  
Vol 299 (6) ◽  
pp. E959-E967 ◽  
Author(s):  
R. L. Anderson ◽  
S. B. Ternes ◽  
K. A. Strand ◽  
M. J. Rowling
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Binding Protein ◽  
Serum Vitamin ◽  
Vitamin D Status ◽  
Vitamin D Binding Protein ◽  
Renal Reabsorption ◽  
Vitamin D Levels ◽  
Zucker Diabetic Fatty Rats ◽  
25 Hydroxycholecalciferol

Altered serum concentrations of the major circulating form of vitamin D [25-hydroxycholecalciferol (25D3)] and its active hormone derivative [1,25-dihydroxycholecalciferol (1,25D3)] have been linked to non-insulin-dependent diabetes mellitus (NIDDM). However, a mechanistic basis for this occurrence has not been fully elucidated. Normally, renal reabsorption of vitamin D-binding protein-bound 25D3 absolutely requires receptor-mediated endocytosis via a receptor complex containing megalin, cubilin, and disabled-2 (Dab2), whereas an absence of megalin or its endocytic partners can lead to a marked urinary loss of 25D and severe vitamin D deficiency. Therefore, we hypothesized that reduced serum vitamin D status in NIDDM may be due to reduced expression of megalin and/or its endocytic partners and increased urinary excretion of protein-complexed 25D3. In the present study, we utilized Zucker diabetic fatty Rats (ZDF) to demonstrate that renal reuptake of the 25D3-DBP complex was compromised in ZDF animals, which was reflected by a reduction in expression of megalin and Dab2. Moreover, serum levels of both 25D3 and 1,25D3 were reduced, and urinary 25D3, 1,25D3, and DBP excretion were elevated in the ZDF animals compared with their lean controls regardless of vitamin D levels in the diet. Taken together, these are the first reports to our knowledge that associate compromised renal reabsorption of the 25D3-DBP complex with expression of megalin and its endocytic partners in NIDDM, which in turn can lead to compromised vitamin D status.

scholarly journals Calcium-binding protein and vitamin D metabolism in experimental protein malnutrition

1974 ◽  
Vol 32 (3) ◽  
pp. 569-578 ◽  
Author(s):  
W. J. Kalk ◽  
B. L. Pimstone
Keyword(s):  
Vitamin D ◽  
Calcium Binding ◽  
Binding Protein ◽  
Calcium Binding Protein ◽  
Protein Deprivation ◽  
Vitamin D Metabolism ◽  
Renal Metabolism ◽  
Acid Substrate ◽  
Amino Acid Substrate ◽  
25 Hydroxycholecalciferol

1. Intestinal and renal vitamin D-dependent calcium-binding protein (CaBP) activity and cholecalciferol metabolism were investigated in the protein-deficient rat (40 g casein/kg diet) and in control animals (200 g casein/kg diet). Compared to control animals, 3 weeks of protein deprivation resulted in consistently reduced intestinal CaBP activity, while renal CaBP activity was not significantly altered.2. Intestinal CaBP activity was greatly reduced in rats fed on diets deficient in both protein and vitamin D. CaBP activity was doubled by cholecalciferol administration, but did not reach control values. The rate of conversion of intravenously injected [3H]cholecalciferol to 25-hydroxycholecalciferol (25-HCC) and the disappearance rates of plasma 25-HCC were similar in the two groups of animals.3. It is concluded that in the protein-deficient rat: (a) intestinal CaBP activity is reduced; (b) coexistent vitamin D deficiency reduces intestinal CaBP activity still further, but the intestinal mucosa retains the potential to respond to administered cholecalciferol: (c) hepatic and probably renal metabolism of cholecalciferol appear to be normal; (d) reduced CaBP is likely to be the result of reduced CaBP synthesis as a consequence of deficient amino acid substrate.

scholarly journals Dietary Resistant Starch Prevents Urinary Excretion of 25-Hydroxycholecalciferol and Vitamin D-Binding Protein in Type 1 Diabetic Rats

2013 ◽  
Vol 143 (7) ◽  
pp. 1123-1128 ◽  
Author(s):  
Anne L. Smazal ◽  
Nicholas C. Borcherding ◽  
Alysse S. Anderegg ◽  
Kevin L. Schalinske ◽  
Elizabeth M. Whitley ◽  
...  
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Resistant Starch ◽  
Binding Protein ◽  
Diabetic Rats ◽  
Vitamin D Binding Protein ◽  
25 Hydroxycholecalciferol

Effect of Phenobarbitone Treatment on Vitamin D Metabolism in Mammals

1974 ◽  
Vol 46 (4) ◽  
pp. 433-448 ◽  
Author(s):  
J. Silver ◽  
G. Neale ◽  
G. R. Thompson
Keyword(s):  
Vitamin D ◽  
Biological Activity ◽  
Silicic Acid ◽  
Vitamin D3 ◽  
Water Soluble ◽  
Prolonged Treatment ◽  
Vitamin D Metabolism ◽  
Silicic Acid Chromatography ◽  
Polar Metabolites ◽  
25 Hydroxycholecalciferol

1. The metabolism of radioactive cholecalciferol was studied in control and phenobarbitone-treated rats and pigs. 2. Treatment with phenobarbitone enhanced the appearance in plasma of 25-hydroxycholecalciferol (peak IV on silicic acid chromatography), and of more-polar metabolites (peak V), but not of the most-polar metabolites (peak VI). Peak IV had the chromatographic properties of authentic 25-hydroxycholecalciferol (25-HCC) and had biological activity. 3. There was no effect on the appearance of peaks V and VI in plasma after an injection of radioactive 25-HCC. 4. Treatment with phenobarbitone enhanced the excretion of metabolites of radioactive vitamin D3 in bile. These metabolites were largely water-soluble conjugates of peaks IV, V and VI, which included glucuronides. Peak IV in bile was not identical with 25-HCC. 5. Prolonged treatment with phenobarbitone depleted the tissue radioactivity of rats given radioactive vitamin D3.

scholarly journals P431 Vitamin D binding protein in the limelight: IBD-related inflammation and circulating levels of vitamin D binding protein, total, free and bioavailable 25-hydroxyvitamin D

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S393-S393
Author(s):  
A Aksan ◽  
K Böttger ◽  
N Hein ◽  
Y Caicedo-Zea ◽  
I Diehl ◽  
...  
Keyword(s):  
Vitamin D ◽  
Binding Protein ◽  
Transferrin Saturation ◽  
Simultaneous Detection ◽  
Full Blood Count ◽  
Vitamin D Binding Protein ◽  
Vitamin D Metabolism ◽  
Hydroxyvitamin D ◽  
Vitamin D Levels ◽  
25 Hydroxyvitamin D

Abstract Background Vitamin D deficiency occurs frequently in patients with Crohn’s disease (CD) and ulcerative colitis (UC). While recent cohort studies support an association of vitamin D with important clinical parameters and outcomes in IBD, the complex interplay of inflammation with vitamin D metabolism in IBD poses a viscious circle. We sought to further illucidate the relation between inflammation and different vitamin D parameters. To the best our knowledge, this was the first study to focus on the relationship between vitamin D binding protein (VDBP), circulating total, free, and bioavailable 25-hydroxyvitamin D (25(OH)D), and inflammation, in adult IBD patients. Methods This was a comparative, single-centred, cross-sectional study in patients with IBD aged 18–65 years. Full blood count, transferrin, albumin and hsCRP were determined by standard methods. The presence/absence of inflammation was assessed based on serum hsCRP levels (cutoff <5mg/l). VDBP levels were determined by ELISA, and 25(OH)D by LCMS. Free and bioavailable vitamin D levels were calculated using the validated formula. IBM SPSS version 25.0 was used for statistical analysis. Results In total, 129 subjects with IBD (70 male/59 female; 82 CD/47 UC; mean age 41.7 ± 12.6 years) were enrolled. Of these, 38/129 had inflammation (19 m/19 f; 26 CD/12 UC; 39.6 ± 12.9 years) while 91/129 had no inflammation (40 m/51 f; 56 CD/35 UC; 42.5 ± 12.5 years). Subjects with disease activity had significantly higher leukocyte, erythrocyte sedimentation rate (ESR) and hsCRP, but lower transferrin, transferrin saturation (TSAT) and albumin levels than those without inflammation (p < 0.05). Average serum levels of 25(OH)D (24.6[6.8–54.8] vs. 26.4[5.0–74.4]ng/ml), free 25(OH)D (5.9[1.3–13.3] vs. 1.0[1.0–21.4]ng/ml) and bioavailable 25(OH)D(2.3 [0.1–4.7] vs. 2.4[0.5–19.5]ng/ml) were similar in patients with vs. without inflammation (p > 0.05). However, VDBP levels were significantly higher in inflammatory conditions (359.6[252.2–530.6] mg/l vs. 327.4[183.5–560.3]mg/l; p < 0.05) and showed a positive correlation with CRP levels (0.293, p < 0.001). Ratio of free/total 25(OH)D correlated negatively with CRP levels (−0.282, p = 0.002). Conclusion High levels of circulating VDBP were associated with inflammatory activity. Moreover, free/total 25(OH)D ratio was inversely associated with inflammation. Other vitamin D parameters including total, free and bioavailable 25(OH)D showed no association with inflammation. These findings suggest that VDBP may play a bigger role than thought as a modulator of vitamin D and inflammation, and that simultaneous detection and investigation of plasma VDBP may provide additional insights into this complex interaction.

Phosphorus adaptation in rats in absence of vitamin D or parathyroid glands

1980 ◽  
Vol 239 (4) ◽  
pp. G261-G265
Author(s):  
C. F. Cramer ◽  
J. McMillan
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Vitamin D Deficiency ◽  
Intestinal Absorption ◽  
Control Diet ◽  
Inorganic Phosphorus ◽  
Parathyroid Glands ◽  
Intestinal Excretion ◽  
Growing Rats ◽  
Pi Deficiency

Growing rats even when vitamin D deficient became adapted to inorganic phosphorus (Pi) deficiency by increasing absorption and minimizing excretion. Feeding low-Pi diet for 3 wk reduced urinary Pi by 80% (P < 0.001), and urinary 32P by 50% (P < 0.001). Low-Pi regimen increased 32p absorption from a 32P-labeled meal by 50% (P < 0.001), even when the animals were vitamin D deficient or thyroparathyroidectomized. The marked increase in retention of 32P in phosphorus-deficient rats could not be accounted for by decreased endogenous intestinal excretion plus increased kidney reabsorption; increased intestinal absorption played a part. 32P absorption was significantly reduced (P < 0.001) by vitamin D deficiency in rats fed either control diet (.6%) Pi or low-Pi diet (0.03%). Endogenous intestinal or urinary excretion of 32P was unaltered by vitamin D deficiency. The evidence supports the hypothesis that there are two mechanisms for phosphorus adaptation: kidney retention not requiring vitamin D, and inreased intestinal absorption of Pi not requiring parathyroids, thyroids, or vitamin D.

Contrasting effects of intravenous and oral etidronate on vitamin D metabolism in man

1988 ◽  
Vol 74 (1) ◽  
pp. 101-106 ◽  
Author(s):  
P. J. Lawson-Matthew ◽  
D. F. Guilland-Cumming ◽  
A. J. P. Yates ◽  
R. G. G. Russell ◽  
J. A. Kanis
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Progressive Increase ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Vitamin D Metabolism ◽  
Dihydroxyvitamin D3 ◽  
Renal Tubular Reabsorption ◽  
Early Effects ◽  
Renal Tubular

1. We have studied the early effects of intravenously and orally administered etidronate on vitamin D metabolism and indirect indices of calcium and skeletal metabolism in 17 patients with Paget's disease of bone. 2. Administration of etidronate by mouth (700–1400 mg daily for 1 month) or its intravenous infusion (300 mg daily for 5 days) decreased bone resorption as judged by urinary excretion of hydroxyproline and significantly increased renal tubular reabsorption of phosphate. No significant change in serum activity of alkaline phosphatase was noted with either regimen. 3. When etidronate was given by mouth there was a progressive decrease in fasting urinary calcium excretion and a rise in serum 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. In contrast, intravenous etidronate decreased serum values of l,25-(OH)2D3 and was associated with a progressive increase in fasting calcium excretion, suggesting a decrease in the net influx of calcium from the extracellular compartment to bone. Significant inverse correlations were noted between the change induced in 1,25-(OH)2D3 values at 2 weeks and the changes in serum calcium, phosphate and fasting urinary excretion of calcium. 4. These observations suggest that the different effects of intravenous and oral etidronate on l,25-(OH)2D3 values are a consequence of different doses of etidronate used and the different effects of these regimens on the accretion of calcium into bone.

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