1,25-Dihydroxyvitamin D3-26,23-lactone interferes in determination of 1,25-dihydroxyvitamin D by RIA after immunoextraction

1995 ◽  
Vol 41 (9) ◽  
pp. 1313-1314 ◽  
Author(s):  
B W Hollis
Keyword(s):  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3

Effects of 1,25-dihydroxyvitamin D3 and cortisol on bovine and human parathyroid cells

1989 ◽  
Vol 123 (1) ◽  
pp. 137-142 ◽  
Author(s):  
R. Karmali ◽  
S. Farrow ◽  
M. Hewison ◽  
S. Barker ◽  
J. L. H. O'Riordan
Keyword(s):  
Parathyroid Hormone ◽  
Receptor Protein ◽  
Mrna Levels ◽  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3 ◽  
Cytosolic Protein

ABSTRACT Incubation of bovine parathyroid cells with 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) decreased both preproparathyroid mRNA levels and parathyroid hormone (PTH) secretion. There was a fall to 56·6 ± 13·7% (mean ± s.e.m.) and 65·1 ± 9·3% in mRNA levels and PTH secretion respectively at 1 nmol 1,25-(OH)2D3/l, and 41·1 ± 13·6% and 42·0 ± 12·1% at 10 nmol 1,25-(OH)2D3/l after 24 h. After 48 h in 0·1 nmol 1,25-(OH)2D3/l, mRNA levels had fallen to 35·3 ± 12·6% and PTH secretion to 32·1 ± 5·0%. In human adenomatous cells, however, incubation with 1,25-(OH)2D3 (10 nmol/l) had no effect on either mRNA levels or PTH secretion even after 48 h. This lack of sensitivity of adenomatous cells to 1,25-(OH)2D3 was not due to an absence of receptors (3847 ± 39 receptors/ng cytosolic protein in adenomatous cells compared with 4068 ± 371 in bovine cells) or receptors being of low affinity. Cortisol (1 μmol/l) caused a reduction in the number of receptors for 1,25-(OH)2D3 in bovine parathyroid cells of approximately 20% within 24 h of incubation, but no change in affinity. This decrease was accompanied by abolition of the response to 1,25-(OH)2D3 and was reversible, in that withdrawal of cortisol for the final 24 h of incubation was sufficient for the response to return, the number of receptors having returned to control values. These results suggest that only a small percentage of receptors for 1,25-(OH)2D3 in bovine parathyroid cells may be functional at any one time. Furthermore, the insensitivity of human adenomatous cells to 1,25-(OH)2D3 does not seem to be due to a lack of receptors but may be due to a defect in the interaction between the receptor protein and the PTH gene. Journal of Endocrinology (1989) 123, 137–142

Effect of 1,25-dihydroxyvitamin D deficiency on the metabolic clearance rate of 1,25-dihydroxyvitamin D3: studies using pigs with vitamin D-dependent rickets type 1

1985 ◽  
Vol 69 (5) ◽  
pp. 549-552
Author(s):  
John Fox ◽  
Anthony D. Care
Keyword(s):  
Vitamin D ◽  
Clearance Rate ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3 ◽  
Steady State Levels

1. We have used pigs with inherited vitamin D-dependent rickets type 1 to study the effect of 1,25-dihydroxyvitamin D deficiency on the metabolic clearance rate of 3H-1,25-dihydroxyvitamin D3 infused to steady-state levels in plasma. 2. Plasma levels of 1,25-dihydroxyvitamin D were 24 ± 1 (sem) pmol/l in the hypocalcaemic, homozygous piglets and 196 ± 27 pmol/l in their normocalcaemic, heterozygous siblings. 3. The metabolic clearance rate of 1,25-dihydroxyvitamin D3 was the same in both normal heterozygous (0.90 ± 0.02) and hypocalcaemic, homozygous piglets (0.90±0.01 ml−1 min−1 kg−1 metabolic bodysize). 4. We conclude that a deficiency of circulating 1,25-dihydroxyvitamin D does not influence the clearance of 1,25-dihydroxyvitamin D3 from the circulation of pigs.

scholarly journals 1,25-Dihydroxyvitamin D3 and Development of Tuberculosis in Cattle

2003 ◽  
Vol 10 (6) ◽  
pp. 1129-1135 ◽  
Author(s):  
S. G. Rhodes ◽  
L. A. Terry ◽  
J. Hope ◽  
R. G. Hewinson ◽  
H. M. Vordermeier
Keyword(s):  
Vitamin D ◽  
T Cell ◽  
Mononuclear Cells ◽  
T Cell Proliferation ◽  
Accessory Cell ◽  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
Cell Responses ◽  
1,25 Dihydroxyvitamin D ◽  
Accessory Cells

ABSTRACT This report describes the presence and activity of 1,25-dihydroxyvitamin D3 (1,25-D3) in experimental bovine tuberculosis. Animals that went on to develop tuberculous lesions exhibited a rapid transient increase in serum 1,25-D3 within the first 2 weeks following infection with Mycobacterium bovis. 1,25-D3-positive mononuclear cells were later identified in all tuberculous granulomas by immunohistochemical staining of postmortem lymph node tissue. These results suggest a role for 1,25-D3 both at the onset of infection and in the development of the granuloma in these infected animals. Using a monoclonal antibody to the vitamin D receptor (VDR) as a VDR agonist, we confirmed that activation of the vitamin D pathway profoundly depresses antigen-specific, but not mitogenic, bovine peripheral blood T-cell responses (proliferation and gamma interferon production). Investigation of the mechanism of this suppression showed that the VDR antibody modified the expression of CD80 by accessory cells, such that a significant positive correlation between T-cell proliferation and accessory cell CD80 emerged.

Hypercalcaemia

2011 ◽  
pp. 642-652
Author(s):  
Ronen Levi ◽  
Justin Silver
Keyword(s):  
Extracellular Fluid ◽  
Immune Functions ◽  
Calcium Sensing Receptor ◽  
Neuromuscular Activation ◽  
Plasma Coagulation ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Calcium Sensing ◽  
Life Threatening

Ionized calcium is essential for several physiological functions, including neuromuscular activation, endocrine and exocrine secretions, integrity of cellular bilayers, plasma coagulation, immune functions and bone metabolism. Extracellular fluid (ECF) calcium is uniquely controlled by its own calcium-sensing receptor, regulating the secretion of parathyroid hormone (PTH), synthesis of 1,25-dihydroxyvitamin D, and the renal reabsorption of filtered calcium (see Chapter 4.1). With the advent of the autoanalyser and routine determination of serum calcium levels, recognition of hypercalcaemia has become common. However, the clinical spectrum of hypercalcaemia varies from a laboratory-detected, asymptomatic mineral disorder to a life-threatening state.

scholarly journals Regulation of Cellular Growth by 1,25-Dihydroxyvitamin D3-Mediated Growth Factor Expression

Physiology ◽  
1999 ◽  
Vol 14 (1) ◽  
pp. 37-40
Author(s):  
Timothy D. Veenstra ◽  
Mark R. Pittelkow ◽  
Rajiv Kumar
Keyword(s):  
Growth Factor ◽  
Cell Types ◽  
Cellular Growth ◽  
Phosphorus Metabolism ◽  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Factor Expression ◽  
Growth Factor Expression ◽  
Different Cell Types

Although the primary function of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] is the regulation of calcium and phosphorus metabolism, it also regulates the growth and differentiation of several different cell types. Recent work suggests that 1,25(OH)2D3 regulates cellular growth by altering the synthesis of growth factors and growth factor responses.

Systemic effects of 1,25-dihydroxyvitamin D3 on the pituitary-hypothalamic axis in rats

1987 ◽  
Vol 115 (2) ◽  
pp. 225-228 ◽  
Author(s):  
K. Törnquist ◽  
C. Lamberg-Allardt
Keyword(s):  
Hormone Secretion ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
25 Hydroxyvitamin D ◽  
Wet Weight ◽  
Indirect Action

Abstract. Treatment of rats with 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) 0.05 μg/kg per day for three days was without any effect on serum T3, T4 or TSH concentrations, whereas serum PRL increased (20.6 ± 3.8 to 76.2 ± 19.1 μg/l, mean ± sem, N = 7–8; P < 0.01). Increased hypothalamic TRH levels (24.3 ± 3.9 to 45.7 ± 7.8 pmol/g wet weight; P < 0.01) may indicate an effect of 1,25(OH)2D3 on hypothalamic TRH homeostasis. This effect could probably be due to an indirect action of 1,25(OH)2D3, mediated by the increased serum calcium (2.77 ± 0.02 to 3.16 ± 0.08 mmol/l, mean ± sem, N = 7–8; P < 0.001). This assumption was, however, not tested. Neither the pituitary TSH nor PRL was affected. The treatment decreased the serum concentration of 25-hydroxyvitamin D3 (23.0 ± 1.3 to 16.8 ± 2.0 nmol/l, mean ± sem, N = 5–7; P < 0.01) and of 24,25-dihydroxyvitamin D3 (3.2 ± 0.3 to 2.1 ± 0.1 nmol/l, mean ± sem, N = 3–5; P < 0.05). The results show that in this experimental design, 1,25(OH)2D3 has no effect on basal hormone secretion from the pituitary-thyroid axis, and that 1,25(OH)2D3 decreases the synthesis of the vitamin D3 metabolites studied.

1,25-Dihydroxyvitamin D3 and TPA activate phospholipase D in Caco-2 cells: role of PKC-α

1999 ◽  
Vol 276 (4) ◽  
pp. G993-G1004 ◽  
Author(s):  
Sharad Khare ◽  
Marc Bissonnette ◽  
Beth Scaglione-Sewell ◽  
Ramesh K. Wali ◽  
Michael D. Sitrin ◽  
...  
Keyword(s):  
Phospholipase D ◽  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Kinase C ◽  
Pkc Isoforms ◽  
Gf 109203X ◽  
Pkc Β ◽  
Stimulation Of

1,25-Dihydroxyvitamin D3[1,25(OH)2D3] and 12- O-tetradecanoylphorbol 13-acetate (TPA) both activated phospholipase D (PLD) in Caco-2 cells. GF-109203x, an inhibitor of protein kinase C (PKC) isoforms, inhibited this activation by both of these agonists. 1,25(OH)2D3activated PKC-α, but not PKC-β1, -βII, -δ, or -ζ, whereas TPA activated PKC-α, -β1, and -δ. Chronic treatment with TPA (1 μM, 24 h) significantly reduced the expression of PKC-α, -βI, and -δ and markedly reduced the ability of 1,25(OH)2D3or TPA to acutely stimulate PLD. Removal of Ca2+ from the medium, as well as preincubation of cells with Gö-6976, an inhibitor of Ca2+-dependent PKC isoforms, significantly reduced the stimulation of PLD by 1,25(OH)2D3or TPA. Treatment with 12-deoxyphorbol-13-phenylacetate-20-acetate, which specifically activates PKC-βI and -βII, however, failed to stimulate PLD. In addition, the activation of PLD by 1,25(OH)2D3or TPA was markedly reduced or accentuated in stably transfected cells with inhibited or amplified PKC-α expression, respectively. Taken together, these observations indicate that PKC-α is intimately involved in the stimulation of PLD in Caco-2 cells by 1,25(OH)2D3or TPA.

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