Feedback Regulation of 25-Hydroxycholecalciferol Metabolism by Vitamin D3

1975 ◽  
Vol 48 (3) ◽  
pp. 227-230
Author(s):  
I. M. A. Evans ◽  
K. W. Colston ◽  
L. Galante ◽  
I. MacIntyre
Keyword(s):  
Vitamin D ◽  
Vitamin D3 ◽  
Actinomycin D ◽  
Feedback Regulation ◽  
Kidney Cells ◽  
Hydroxylase Activity ◽  
25 Hydroxycholecalciferol

1. In vitamin D-deficient chicks both vitamin D3 and 1α-hydroxycholecalciferol markedly decrease renal 1-hydroxylase activity and induce 24-hydroxylase activity. 2. Actinomycin D abolishes both effects. 3. These results are consistent with feedback regulation of vitamin D3 metabolism by a direct nuclear action of the vitamin or its metabolites on the kidney cells.

scholarly journals Effect of oestrogen and 1,25-dihydroxycholecalciferol on 25-hydroxycholecalciferol metabolism in primary chick kidney-cell cultures

1978 ◽  
Vol 174 (1) ◽  
pp. 231-236 ◽  
Author(s):  
E Spanos ◽  
D I Barrett ◽  
K T Chong ◽  
I MacIntyre
Keyword(s):  
Vitamin D ◽  
Cell Cultures ◽  
Kidney Cell ◽  
Primary Cultures ◽  
Kidney Cells ◽  
Hydroxylase Activity ◽  
Experimental Conditions ◽  
Polar Metabolites ◽  
Chick Kidney ◽  
25 Hydroxycholecalciferol

Primary cultures of chick kidney cells convert 25-hydroxycholecalciferol into more-polar metabolites. Cells from vitamin D-deficient chicks have high 25-hydroxycholecalciferol 1 alpha-hydroxylase (1 alpha-hydroxylase) activity, but no 25-hydroxycholecalciferol 24-hydroxylase (24-hydroxylase) activity. Physiological concentrations of 1,25-dihydroxycholeclaciferol suppress 1 alpha-hydroxylase and induce 24-hydroxylase activity. The inhibition of 1 alpha-hydroxylase preceded the induction of 24-hydroxylase. In contrast, oestradiol-17 beta had no effect on the activity of either hydroxylase under a variety of experimental conditions. These results clearly demonstrate that 1,25-dihydroxycholecalciferol, but not oestrogen, acts directly on the kidney cells to regulate the metabolism of 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 Feedback regulation of vitamin D metabolism by 1,25-dihydroxycholecalciferol

1977 ◽  
Vol 164 (1) ◽  
pp. 83-89 ◽  
Author(s):  
K W Colston ◽  
I M A Evans ◽  
T C Spelsberg ◽  
I MacIntyre
Keyword(s):  
Vitamin D ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Gene Transcription ◽  
Subcutaneous Administration ◽  
Feedback Regulation ◽  
Rna Polymerase I ◽  
Hydroxylase Activity ◽  
Vitamin D Metabolism ◽  
Polymerase I

Many factors influence the production of 1,25(OH)2D3 (1,25-dihydroxycholecalciferol) by the kidney. One important factor seems to be feedback regulation by 1,25(OH)2D3 itself. Administration of 1,25(OH)2D3 to vitamin D-deficient chicks abolishes renal 25(OH)D3(25-hydroxycholecalciferol)1-hydroxylase activity and induces the appearance of 25(OH)D3 24-hydroxylase activity. It is likely that these effects are mediated via a nuclear effect, as they are prevented by pretreatment with actinomycin D and alpha-amanitin. Further, 1,25(OH)2D3 has a marked effect on gene transcription in the kidney cell, as assessed by measurement of RNA polymerase activities. RNA polymerase I and II activities are 80-90% inhibited by 12.5nmol of 1,25(OH)2D3 within 30min of subcutaneous administration, indicating an immediate and massive decrease in total gene transcription. By 4h RNA polymerase II activity has returned to control values, but RNA polymerase I activity is markedly enhanced. These results are consistent with the view that regulation of cholecalciferol metabolism in the kidney is associated with an effect of the active metabolite on the kidney nucleus.

Submitochondrial localization of kidney 25-hydroxycholecalciferol 1α-hydroxylase in vitamin D repleted weanling guinea pigs

1987 ◽  
Vol 65 (7) ◽  
pp. 673-676 ◽  
Author(s):  
Xue Yan ◽  
Guy Charette ◽  
Edgard E. Delvin
Keyword(s):  
Vitamin D ◽  
Cytochrome C ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Membrane Fraction ◽  
Hydroxylase Activity ◽  
Oxidoreductase Activity ◽  
Pig Kidney ◽  
Steroid Hydroxylases ◽  
25 Hydroxycholecalciferol

We have studied the submitochondrial localization of guinea-pig kidney 25-hydroxycholecalciferol 1α-hydroxylase. Treatment of the mitochondrial-enriched fraction with recrystallized digitonin produced mitoplasts bordered by a single membrane and with intact matrix. They contained nearly 90% of the 25-hydroxycholecalciferol 1α-hydroxylase activity and nearly 100% of the cytochrome-c: oxygen oxidoreductase. Amine: oxygen oxidoreductase activity remained mainly in the outer membrane fraction. These data show that 25-hydroxycholecalciferol 1α-hydroxylase has a distribution similar to that of steroid hydroxylases.

The Effects of a Diphosphonate and Dietary Calcium on the Metabolism of Vitamin D3 (Cholecalciferol) in the Chick

1975 ◽  
Vol 49 (5) ◽  
pp. 391-400
Author(s):  
Carol M. Taylor ◽  
E. Barbara Mawer ◽  
A. Reeve
Keyword(s):  
Vitamin D ◽  
Oral Dose ◽  
Single Oral Dose ◽  
Vitamin D3 ◽  
Dietary Calcium ◽  
No Inhibition ◽  
25 Hydroxycholecalciferol

1. Vitamin D-deficient chicks, maintained on a diet adequate in calcium and treated with ethane-1-hydroxy-1,1-diphosphonate for 2 days before a single oral dose of cholecalciferol (vitamin D3), converted the vitamin into 24,25-dihydroxycholecalciferol instead of into the normal metabolite 1,25-dihydroxycholecalciferol. 2. This inhibition of the renal 1-hydroxylase disappeared on withdrawal of the diphosphonate. 3. Kidneys from chicks given diphosphonate for 12 days converted 25-hydroxycholecalciferol into 24,25-dihydroxycholecalciferol on incubation in vitro. 4. The inhibition of the 1-hydroxylase was markedly accelerated by treating the birds with cholecalciferol. 5. No inhibition of renal 1-hydroxylation was observed in birds maintained on a diet low in calcium. 6. A possible mechanism producing this effect is discussed.

The effect of dietary calcium on the activity of 25-hydroxycholecalciferol-l-hydroxylase and Ca absorption in vitamin D-replete chicks

1977 ◽  
Vol 38 (1) ◽  
pp. 47-54 ◽  
Author(s):  
R. Swaminathan ◽  
Barbara A. Sommerville ◽  
A. D. Care
Keyword(s):  
Vitamin D ◽  
Dietary Intake ◽  
Specific Activity ◽  
Dietary Calcium ◽  
Duodenal Mucosa ◽  
List Type ◽  
Type Number ◽  
Hydroxylase Activity ◽  
Dietary Level ◽  
25 Hydroxycholecalciferol

1.As most of the studies on the regulation of renal 25-hydroxycholecalciferol-1-hydroxylase (25-HCC-1-hydroxylase) activity have been done in marginally-vitamin D-defieient animals and as it is known that vitamin D administration suppresses the specific activity of the 25-HCC-1-hydroxylase, it was decided to study the effect of dietary calcium on the activity of 25-HCC-1-hydroxylase and on Ca absorption in vitamin Dreplete chicks.2.Chicks, 10 d old, were given diets differing in their Ca contents (65 nmol cholecalciferol/kg diet) for 10 d and the activity of 25-HCC-1-hydroxylase in kidney homogenates, Ca absorption from the duodenum, Cabinding protein (CaBP) activity in the duodenal mucosa and plasma Ca and phosphate concentrations were all determined.3.The CaBP activity and the efficiency of Ca absorption both decreased with increasing dietary intake of Ca. Ca absorption and CaBP activity were significantly correlated (r 0.995, P < 0.01).4.The activity of 25-HCC-1-hydroxylase decreased as the dietary level of Ca increased and was significantly correlated with Ca absorption (r0.900, P < 005). The plasma Ca concentration and the activity of 25-HCC-1-hydroxylase were inversely related (r-0.940, P < 0.01).5.It is concluded that in the vitamin D-replete chick the efficiency of duodenal Ca absorption is regulated by the renal 25-HCC-1-hydroxylase activity via production of 1,25-dihydroxycholecalciferol and CaBP synthesis.

scholarly journals Correlation of vitamin D3 and serum calcium level with left ventricular hypertrophy patients.

2020 ◽  
Vol 27 (06) ◽  
pp. 1143-1150
Author(s):  
Masood Nabi Noor ◽  
Anawar Ali Jamali ◽  
Hajra Naila Rahu ◽  
Ghulam Mustafa Jamali ◽  
Altaf Hussain Memon ◽  
...  
Keyword(s):  
Vitamin D ◽  
Essential Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Serum Calcium ◽  
Vitamin D3 ◽  
Ventricular Hypertrophy ◽  
Serum Vitamin ◽  
Left Ventricular ◽  
Serum Vitamin D ◽  
25 Hydroxycholecalciferol

Extra cellular fluid (ECF) Ca++ performs vital functions such as blood clotting, cardiac muscle contraction, second messenger for hormone and neurotransmitter release. Total Ionized serum Ca++ is 4.65 to 5.25 mg/dl Ionized Ca++ performs vital physiological functions such as maintenance of plasma membrane integrity. Objectives: The present study is the first research being reporting on the association of LVH (left ventricular hypertrophy) due to essential hypertension with serum vitamin D3 and serum calcium levels. Study Design: Cross Sectional Research. Setting: Medicine/Cardiology department, Peoples Medical University Hospital, Nawabshah. Period: 1st January 2017 to 30th June 2017. Material & Methods: To assess the correlation of 25-hydroxycholecalciferol and serum calcium with left ventricular hypertrophy in essential hypertension. The thickness of inter ventricular septum (IVS) and posterior wall (PWT) on echocardiography were used to categorize LVH into mild, moderate and severe. Results: Male predominated in the present study. Male to female ratio was 1.65:1. Male and female comprised 62.33% and 37.67% respectively. Chi square value (X2-value) was 14.7 with significant p-value. Mean +SD of 25-hydroxycholecalciferol in mild moderate and severe LVH were noted as 30+7.8, 24.7+7.7 and 14.9+6.1 ng/dl respectively. Mean +SD of serum calcium in mild moderate and severe LVH were noted as 9.20+0.51, 8.93+0.72 and 8.678+0.44 mg/dl respectively. Conclusion: In subjects with left ventricular hypertrophy in essential hypertension the serum levels of vitamin D and calcium were low. There was a negative correlation with left ventricular hypertrophy and serum vitamin D and serum calcium. Thus it could be concluded that in subjects with left ventricular hypertrophy the low levels of serum vitamin D could be an independent modifiable risk factor.

Vitamin D Metabolism in Adult Rats at Low and Normal Calcium Intake and the Effect of Cadmium Exposure

1977 ◽  
Vol 53 (5) ◽  
pp. 439-446
Author(s):  
R. Lorentzon ◽  
S.-E. Larsson
Keyword(s):  
Vitamin D ◽  
Dietary Intake ◽  
Intestinal Mucosa ◽  
Vitamin D3 ◽  
Calcium Intake ◽  
Dietary Calcium ◽  
Cadmium Exposure ◽  
Dietary Calcium Intake ◽  
Adult Rats ◽  
25 Hydroxycholecalciferol

1. Chromatography measurements indicated that adult rats converted 25-hydroxycholecalciferol into 1,25-dihydroxycholecalciferol at a lower rate than that reported earlier for young animals. In serum, less-polar metabolites were found which probably represented vitamin D esters and vitamin D3. 2. A low dietary intake of calcium resulted in an evident increase in the fraction corresponding to 1,25-dihydroxycholecalciferol in the kidneys and also in the intestinal mucosa and serum. 3. Inclusion of 0·67 mmol of cadmium/l of drinking water at a low dietary intake of calcium resulted in an increased accumulation of both cadmium and zinc in the kidneys and liver compared with values at a normal dietary calcium intake. 4. At a normal dietary calcium intake, cadmium exposure caused inhibited production of 1,25-dihydroxycholecalciferol by the kidneys and an increased accumulation of 24,25-dihydroxycholecalciferol, vitamin D3 and vitamin D esters in the serum. 5. The inhibitory effect of cadmium on the renal conversion of 25-hydroxycholecalciferol into 1,25-dihydroxycholecalciferol was almost completely counteracted by a simultaneous low dietary calcium intake. Cadmium-exposed, calcium-deficient animals also showed a maintained accumulation of 1,25-dihydroxycholecalciferol in the intestinal mucosa.

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