Effect of 1,25-dihydroxyvitamin D3 on rat pituitary prolactin release

1987 ◽  
Vol 116 (4) ◽  
pp. 459-464 ◽  
Author(s):  
Kid Törnquist
Keyword(s):  
Pituitary Cells ◽  
Dihydroxyvitamin D3 ◽  
Enhancing Effect ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
Rat Pituitary ◽  
25 Hydroxyvitamin D ◽  
Pituitary Prolactin

Abstract. The effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on PRL secretion from rat pituitary in vivo and in vitro was investigated. Treating the rats for three days with 0.05 μg/kg per day had no effect on basal PRL secretion, whereas the TRH-induced PRL secretion was increased (P < 0.001). The enhancing effect of 1,25(OH)2D3 was blunted by verapamil. Incubating dispersed anterior pituitary cells with 10−8 mol/l 1,25(OH)2D3 induced a significant increase in PRL secretion after 96 h (364 ± 30 ng/well vs 481 ± 33 ng/well, P < 0.001; mean ± sem) compared with control cells. The TRH-induced PRL secretion was increased in cells incubated with 1,25(OH)2D3 for 144 h (0.766 ± 0.061 vs 1.024 ± 0.076 μg/well, P < 0.05; mean ± sem) compared with control cells. Neither 25-hydroxyvitamin D3 (25OH-D3) nor 24,25-dihydroxyvitamin D3 had any effects on the PRL secretion. However, when the cells were incubated with both 10−8 mol/l 1,25(OH)2D3 and 10−6 mol/l 25OHD3, the enhancing effect of 1,25(OH)2D3 on the basal PRL secretion was blunted. The results suggest that 1,25(OH)2D3 possibly affects the regulation of PRL release from the rat pituitary and that this effect is specific for 1,25(OH)2D3.

Role of 25-hydroxyvitamin D3 dose in determining rat 1,25-dihydroxyvitamin D3 production

1990 ◽  
Vol 258 (5) ◽  
pp. E780-E789 ◽  
Author(s):  
R. Vieth ◽  
K. McCarten ◽  
K. H. Norwich
Keyword(s):  
Specific Activity ◽  
Metabolic Clearance ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
25 Hydroxyvitamin D ◽  
Dose Dependent

To understand the relationships among 1) the dose of 25-hydroxyvitamin D [25(OH)D] in vivo, 2) the activity of 1-hydroxylase in renal mitochondria, and 3) the production of 1,25-dihydroxyvitamin D [1,25(OH)2D] in vivo, we gave rats different chronic or acute doses of 25-hydroxyvitamin D3 [25(OH)D3]. We followed the metabolism of intracardially administered [25-hydroxy-26,27-methyl-3H]cholecalciferol [25(OH)[3H]D3] for 24 h before killing by measuring extracts of serum by chromatography. Specific activity of 1-hydroxylase in kidney was measured at death. In rats given 0-2,000 pmol 25(OH)D3 chronically by mouth, there was a dose-dependent decline in the percent of serum radioactivity made up of 1,25-dihydroxy-[26,27-methyl-3H]cholecalciferol [1,25(OH)2[3H]D3] as well as a decline in mitochondrial 1-hydroxylase, and these correlated significantly (r = 0.83, P less than 0.001). Serum %1,25(OH)2[3H]D3 in this experiment ranged from 0.8 to 42%. A small part of this range could be accounted for by a faster metabolic clearance rate (MCR) of 1,25(OH)2D3 from rats supplemented with 25(OH)D3 (MCR, 2.12 +/- 0.10 ml/min) compared with rats restricted in vitamin D (MCR, 0.94 +/- 0.06 ml/min, P less than 0.001). The activity of 1-hydroxylase was by far the major factor determining serum %1,25(OH)2[3H]D3. When different acute doses of 25(OH)D3 were given to rats with identical specific activities of 1-hydroxylase, the resulting 1,25(OH)2D3 concentrations in serum correlated with the 25(OH)D3 dose (r = 0.99, P less than 0.001). We conclude that the behavior of 1-hydroxylase in vivo is analogous to the classic behavior in vitro of an enzyme functioning below its Michaelis constant (Km). The amount of 1-hydroxylase present in renal mitochondria determines the fraction (not simply the quantity) of 25(OH)D metabolized to 1,25(OH)2D3 in vivo.

Effects of tri-iodothyronine, cortisol and transcriptional inhibitors on vitamin D3-enhanced thyrotrophin secretion by rat pituitary cells in vitro

1989 ◽  
Vol 121 (3) ◽  
pp. 451-458 ◽  
Author(s):  
M. C. d'Emden ◽  
J. D. Wark
Keyword(s):  
Primary Cultures ◽  
Relative Increase ◽  
Pituitary Cells ◽  
Dihydroxyvitamin D ◽  
Rat Pituitary ◽  
Tsh Secretion ◽  
Dependent Inhibition ◽  
Rat Pituitary Cells

ABSTRACT The hormone 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) has been shown to selectively enhance agonist-induced TSH release in the rat thyrotroph in vitro. The interaction of 1,25-(OH)2D3 with tri-iodothyronine (T3) and cortisol was studied in primary cultures of dispersed anterior pituitary cells. TRH (1 nmol/l)-induced TSH release over 1 h was enhanced by 70% (P<0·01) following exposure to 10 nmol 1,25-(OH)2D3/l for 24 h. Pretreatment with T3 (1 pmol/l–1 μmol/l) for 24 h caused a dose-dependent inhibition of TRH-induced TSH release. Net TRH-induced TSH release was inhibited by 85% at T3 concentrations of 3 nmol/l or greater. Co-incubation with 1,25-(OH)2D3 resulted in enhanced TRH-induced TSH release at all T3 concentrations tested (P<0·001). The increment of TRH-induced TSH release resulting from 1,25-(OH)2D3 pretreatment was equivalent in the presence or absence of maximal inhibitory T3 concentrations. At 1 nmol T3/1, there was a two- to threefold relative increase in 1,25-(OH)2D3-enhanced TRH-induced TSH release. Incubation with cortisol (100 pmol/l–100 nmol/l) had no effect on basal or TRH-induced TSH release, nor did it alter 1,25-(OH)2D3-enhanced TRH-induced TSH release when added 24 h before, or at the time of addition of 1,25-(OH)2D3. Actinomycin D and α-amanitin abolished 1,25-(OH)2D3-enhanced TSH secretion. These data demonstrate that the action of 1,25-(OH)2D3 in the thyrotroph required new RNA transcription, and was not affected by cortisol. In the presence of T3, the response of the thyrotroph to TRH induced by 1,25-(OH)2D3 was increased. We have shown that 1,25-(OH)2D3 has significant effects on the action of TRH and T3 in vitro. These findings support the proposal that 1,25-(OH)2D3 may modulate TSH secretion in vivo. Journal of Endocrinology (1989) 121, 451–458

1,25-Dihydroxyvitamin D3 downregulates the rat intestinal vitamin D3-25-hydroxylaseCYP27A

2001 ◽  
Vol 281 (2) ◽  
pp. E315-E325 ◽  
Author(s):  
Catherine Theodoropoulos ◽  
Christian Demers ◽  
Ali Mirshahi ◽  
Marielle Gascon-Barré
Keyword(s):  
Vitamin D ◽  
Direct Action ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
Protein Levels ◽  
25 Hydroxyvitamin D ◽  
Extrahepatic Tissues ◽  
Mrna Half Life

The vitamin D3-25-hydroxylase CYP27A is located predominantly in liver, but its expression is also detected in extrahepatic tissues. Our aim was to evaluate the regulation of CYP27A by vitamin D3 (D3) or its metabolites in rat duodena. Vitamin D-depleted rats were repleted with D3, 25-hydroxyvitamin D (25OHD), or 1,25-dihydroxyvitamin D3[1,25(OH)2D3] or acutely injected 1,25(OH)2D3 to investigate the mechanisms of action of the hormone. All D3 compounds led to a progressive decrease in CYP27A mRNA, with levels after D3 representing 20% of that observed in D depletion. 25OHD decreased CYP27A mRNA by 55%, whereas 1,25(OH)2D3 led to a 40% decrease, which was accompanied by a 31% decrease in CYP27A protein levels and an 89% decrease in enzyme activity. Peak circulating 1,25(OH)2D3 concentrations were, however, the highest in D3-repleted, followed by 25OHD- and 1,25(OH)2D3-repleted animals. 1,25(OH)2D3 resulted in a decrease in both CYP27A mRNA half-life and transcription rate. Our data illustrate that the intestine expresses the D3-25-hydroxylase and that the gene is highly regulated in vivo through a direct action of 1,25(OH)2D3 or through the local production of D3 metabolites.

Metabolism of 25-hydroxyvitamin D3 to 24,25-dihydroxyvitamin D3 and its sensitivity to ketoconazole in 1α,25-dihydroxyvitamin D3-differentiated HL60 cells

1989 ◽  
Vol 3 (3) ◽  
pp. 199-205 ◽  
Author(s):  
M. E. Hayes ◽  
D. Bayley ◽  
E. B. Mawer
Keyword(s):  
High Performance ◽  
Cell Number ◽  
Dependent Manner ◽  
Macrophage Phenotype ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
25 Hydroxyvitamin D ◽  
Dose Dependent

ABSTRACT Regulation of the metabolism of [3H]25-hydroxyvitamin D3 ([3H]25-(OH)D3) in vitro to material with the characteristics of [3H]24,25-dihydroxyvitamin D3 ([3H]24,25-(OH)2D3) has been studied in the human promyelocytic cell line HL60. Synthesis of 24,25-(OH)2D3 was induced in a dose-dependent manner in cells pretreated with 0·1–100 nm 1α,25-dihydroxyvitamin D3 (1α,25-(OH)2D3) for 4 days. This treatment also inhibited cell proliferation and stimulated differentiation to a macrophage phenotype that was characterized by staining for non-specific esterase (NSE) activity. The ability to synthesize [3H]24,25-(OH)2D3 from [3H]25-(OH)D3 and the expression of NSE activity both responded to changes in concentration of 1α,25-(OH)2D3 in the culture medium in a parallel manner. Synthesis of [3H]24,25-(OH)2D3 was linear when the incubation time was between 1 and 8 h and the cell number between 1 and 12×106 cells/incubation. The optimum substrate concentration for its synthesis was 125 nm, giving an apparent Michaelis constant of 360 nm. The identity of the [3H]24,25-(OH)2D3 synthesized by these cells was confirmed by co-chromatography with authentic 24,25-(OH)2D3 on normal-phase and reverse-phase high-performance liquid chromatography systems and by its reaction to sodium-m-periodate. Cells that had been exposed to 100 nm 1α,25-(OH)2D3 for 4 days synthesized 2·17±0·07 (s.e.m.) pmol 24,25-(OH)2D3/106 cells per h. This synthesis was inhibited in a dose-dependent manner over a concentration range of 0·01–1 μm by the drug ketoconazole, an antimycotic imidazole which is a known inhibitor of certain cytochrome P-450 enzyme systems, suggesting that the HL60 25-(OH)D3-24-hydroxylase is also a P-450-dependent enzyme system.

Increased Circulatory Extrarenal 1α,25-Dihydroxyvitamin D3 in Bilaterally Nephrectomized Rats

2020 ◽  
Vol 20 (9) ◽  
pp. 1523-1530
Author(s):  
Murat Dabak ◽  
Durrin O. Dabak ◽  
Tuncay Kuloglu ◽  
Ersoy Baydar ◽  
Hakan Bulut ◽  
...  
Keyword(s):  
Immune Cells ◽  
Low Dose ◽  
Systemic Circulation ◽  
Bilateral Nephrectomy ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
Inflammatory Conditions ◽  
Calcium Phosphorus ◽  
25 Hydroxyvitamin D

Background: Extrarenal 1α,25-dihydroxyvitamin D3 (1,25-D) locally produced by immune cells plays crucial roles in the regulation of the immune system. However, in vivo status of extrarenal 1,25-D and 25-hydroxyvitamin D (25-D) in acute inflammatory conditions are unknown. Objective: The aim of this study was to determine the extrarenal 1,25-D level in circulation in bilaterally nephrectomized rats, induced by low-dose lipopolysaccharide (LPS). Methods: Renal 1,25-D synthesis was terminated through bilateral nephrectomy in rats. The rats received intraperitoneal LPS (50 μg/kg BW) three times and the experiment was ended 24 hours after nephrectomy. Serum 1,25-D, 25-D, calcium, phosphorus, intact parathyroid hormone, and calcitonin levels were measured and immunohistochemistry was applied to detect the sources of extrarenal 1,25- D synthesis. Results: Circulatory 1,25-D concentration remarkably increased in both LPS-treated and non-treated bilaterally nephrectomized rats. Elevated circulatory 1,25-D did not have hypercalcemic endocrinal effects. The increased 1,25-D level also resulted in a concurrent rapid and dramatic depletion of circulatory 25-D. Conclusions: Extrarenal 1,25-D could enter into the systemic circulation and, therefore, might have systemic effects besides its autocrine and paracrine functions.

1α,25-dihydroxyvitamin D3 corrects osteomalacia in hypoparathyroidism and pseudohypoparathyroidism

1983 ◽  
Vol 103 (2) ◽  
pp. 241-247 ◽  
Author(s):  
Sol Epstein ◽  
Pierre J. Meunier ◽  
Phillip W. Lambert ◽  
Paula H. Stern ◽  
Norman H. Bell
Keyword(s):  
Serum Calcium ◽  
Inorganic Phosphate ◽  
Binding Assay ◽  
Bone Biopsy ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
Before And After ◽  
25 Hydroxyvitamin D ◽  
Serum Inorganic Phosphate

Abstract. Deficiency of circulating 1α,25-dihydroxyvitamin D (1α,25(OH)2D) regularly occurs in hypoparathyroidism (HP) and pseudohypoparathyroidism (PHP). Osteomalacia is occasionally found in the two diseases. Two patients, one with HP and the other with PHP, both with symptomatic and biopsy-proven osteomalacia, were studied before and after treatment with 1α,25(OH)2D3. Laboratory values before treatment were as follows: serum immunoreactive parathyroid hormone was undetectable in the patient with HP and was elevated in the patient with PHP. Serum 25-hydroxyvitamin D, measured by binding assay, was 131.5 and 61.9 nmol/l (normal: 69.1 ± 15.9 nmol/l); serum 24,25-dihydroxyvitamin D, measured by binding assay, was 13.9 and 3.8 nmol/l (normal: 3.4 ± 1.4 nmol/l); serum 1α,25(OH)2D, measured by bioassay, was 28.6 and 29.0 pmol/l (normal: 77.3 ± 22.8 pmol/l) and, measured by receptor assay, was 36.2 and 41.0 pmol/l (normal: 71.8 ± 35.8 pmol/l) in the HP and PHP patients, respectively. Serum calcium was low and serum inorganic phosphate was high in both cases. Treatment with 1α,25(OH)2D3 (3–5 μg per day for 10–12 months) restored serum calcium and inorganic phosphate to normal, alleviated bone pain and healed the osteomalacia as shown on repeat bone biopsy. Our results provide further evidence that isolated deficiency of 1α,25(OH)2D may cause osteomalacia or rickets.

Oxytocin has a role in gonadotrophin regulation in rats

1990 ◽  
Vol 125 (3) ◽  
pp. 425-432 ◽  
Author(s):  
G. Robinson ◽  
J. J. Evans
Keyword(s):  
Follicular Development ◽  
Pituitary Cells ◽  
Lh Surge ◽  
Rat Pituitary ◽  
Lh Release ◽  
Rat Pituitary Cells ◽  
Dose Dependent ◽  
In Vivo Administration

ABSTRACT We previously demonstrated that oxytocin stimulates LH release from rat pituitary cells in vitro and advances follicular development and ovulation in mice in vivo. This study reports an investigation of rat LH levels following in-vivo administration of oxytocin. Injection of oxytocin (10 mIU/g, i.p.) to rats at 07.00, 08.00 and 09.00 h of pro-oestrus or at 09.00, 10.00 and 11.00 h of pro-oestrus advanced the onset of the LH surge (P<0.005) and attainment of peak concentrations of LH (P<0.02) in peripheral blood. On the other hand, the descending phase of the LH surge and the surge amplitude were not altered by oxytocin. Treatment at 05.00, 06.00 and 07.00 h of pro-oestrus or at 11.00, 12.00 and 13.00 h of pro-oestrus had no effect on the LH profile. A higher oxytocin dose (20 mIU/g) inhibited LH release when treatment was begun at 05.00, 07.00 or 09.00 h of pro-oestrus. A lower dose (5 mIU/g) was ineffective in altering LH concentrations. In addition, injections of oxytocin (10 mIU/g) at oestrus, metoestrus or dioestrus had no effect on the release of LH. Thus the efficacy of oxytocin in altering concentrations of LH was dose dependent and also critically affected by the day of the oestrous cycle and the time of pro-oestrus. Removal of endogenous oxytocin activity by the use of an oxytocin receptor antagonist abolished the pro-oestrous LH surge, indicating that oxytocin is a vital physiological component of the LH-releasing mechanism in rats. The study provides unequivocal evidence that oxytocin induces LH release in vivo, but the manifestation of oxytocin activity is dependent upon conditions of exposure. Journal of Endocrinology (1990) 125, 425–432

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.

Effect of long-term corticosteroid administration on rat pituitary growth hormone and prolactin

1985 ◽  
Vol 108 (4) ◽  
pp. 475-478 ◽  
Author(s):  
R. Oosterom ◽  
T. Verleun ◽  
J. Zuiderwijk ◽  
P. Uitterlinden ◽  
S. W. J. Lamberts
Keyword(s):  
Pituitary Cells ◽  
Corticosteroid Administration ◽  
Pituitary Growth Hormone ◽  
Significant Stimulation ◽  
Rat Pituitary ◽  
Hydrocortisone Administration ◽  
Plasma Gh

Abstract. In vitro corticosteroids stimulate GH synthesis by pituitary cells, while in vivo they suppress stimulated plasma GH levels. In this study we investigated in rats the effect of hydrocortisone administration for 2–4 weeks on pituitary GH content. Hydrocortisone added to the drinking water (100 mg/l) resulted in a marked stimulation of pituitary GH content after 3 and 4 weeks of treatment. No significant stimulation, however, was observed on basal GH release by the pituitary gland incubated in vitro. Further, we found that both Prl content and release were inhibited by hydrocortisone administration.

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