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פותח על ידי קלירמאש פתרונות בע"מ -
Interaction between calcium and 1, 25-dihydroxyvitamin d3 in the regulation of preproparathyroid hormone and vitamin d receptor messenger ribonucleic acid in avian parathyroids
Year:
1993
Source of publication :
Endocrinology
Authors :
בר, אריה
;
.
הורביץ, שמואל
;
.
Volume :
132
Co-Authors:
Russell, J., Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, 10461, United States
Bar, A., Institute of Animal Science, The Volcani Center, Bet Dagan, Israel
Hurwitz, S., Institute of Animal Science, The Volcani Center, Bet Dagan, Israel
Facilitators :
From page:
2639
To page:
2644
(
Total pages:
6
)
Abstract:
Regulation of prepro-PTH and vitamin D receptor (VDR) mRNAs in the parathyroid glands was studied in chickens in vivo. The birds were raised to 21 days of age on a vitamin D-deficient diet with 1% calcium and 0. 65% phosphorous. At the end of this period, the chicks exhibited marked hypocalcemia and enlarged parathyroid glands. In three separate trials, the birds were repleted for 6 days with vitamin D and different dietary calcium and phosphate concentrations, with 2 μg/kg 1, 25-dihydroxyvitamin D3[l, 25-(OH)2D3] and different dietary calcium concentrations (0. 5%, 1. 0%, or 1. 8%), or with 2 or 10 μg/kg 1, 25-(OH)2D3 and 0. 6% or 1. 9% calcium or were kept vitamin D;l deficient and fed 0. 5%, 1. 0%, or 1. 8% dietary calcium. Vitamin D treatment when combined with a high level of dietary calcium resulted in an increase in plasma calcium from 6 mg/dl to greater than 10 mg/dl, a decrease in PTH mRNA of 65%, and a 6- to 8-fold increase in VDR mRNA. In another experiment in which no vitamin D source was given and the diets contained increasing levels of dietary calcium, plasma calcium increased significantly (5. 5 vs. 7 mg/dl), while PTH mRNA decreased by 40% and VDR mRNA increased by 60%. Neither parathyroid gland weight nor total RNA was significantly affected. When chicks were repleted with l, 25-(OH)2D3, the increase in plasma calcium and VDR mRNA and the decrease in PTH mRNA were considerably more pronounced than those in the absence of the vitamin D source. Furthermore, in the presence of the hormone, parathyroid weight and total RNA decreased significantly with increasing concentrations of dietary calcium. When the chicks were repleted, respectively, with the two levels of l, 25-(OH)2D3, a marked positive interaction was evident between the hormone and dietary calcium in affecting levels of PTH and VDR mRNA. These results suggest that both l, 25-(OH)2D3 and calcium participate in the regulation of PTH and VDR gene transcription in the avian parathyroid gland. Whereas the action of 1, 25-(OH)2D3requires a minimal level of dietary calcium, calcium affects PTH and VDR gene transcription even in the absence of any vitamin D source. © 1993 by The Endocrine Society.
Note:
Related Files :
Animal
animal tissue
calcitriol
calcitriol receptor
calcium metabolism
Chickens
hormone precursor
Male
Parathyroid Glands
עוד תגיות
תוכן קשור
More details
DOI :
10.1210/endo.132.6.8389284
Article number:
0
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
18463
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:21
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Scientific Publication
Interaction between calcium and 1, 25-dihydroxyvitamin d3 in the regulation of preproparathyroid hormone and vitamin d receptor messenger ribonucleic acid in avian parathyroids
132
Russell, J., Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, 10461, United States
Bar, A., Institute of Animal Science, The Volcani Center, Bet Dagan, Israel
Hurwitz, S., Institute of Animal Science, The Volcani Center, Bet Dagan, Israel
Interaction between calcium and 1, 25-dihydroxyvitamin d3 in the regulation of preproparathyroid hormone and vitamin d receptor messenger ribonucleic acid in avian parathyroids
Regulation of prepro-PTH and vitamin D receptor (VDR) mRNAs in the parathyroid glands was studied in chickens in vivo. The birds were raised to 21 days of age on a vitamin D-deficient diet with 1% calcium and 0. 65% phosphorous. At the end of this period, the chicks exhibited marked hypocalcemia and enlarged parathyroid glands. In three separate trials, the birds were repleted for 6 days with vitamin D and different dietary calcium and phosphate concentrations, with 2 μg/kg 1, 25-dihydroxyvitamin D3[l, 25-(OH)2D3] and different dietary calcium concentrations (0. 5%, 1. 0%, or 1. 8%), or with 2 or 10 μg/kg 1, 25-(OH)2D3 and 0. 6% or 1. 9% calcium or were kept vitamin D;l deficient and fed 0. 5%, 1. 0%, or 1. 8% dietary calcium. Vitamin D treatment when combined with a high level of dietary calcium resulted in an increase in plasma calcium from 6 mg/dl to greater than 10 mg/dl, a decrease in PTH mRNA of 65%, and a 6- to 8-fold increase in VDR mRNA. In another experiment in which no vitamin D source was given and the diets contained increasing levels of dietary calcium, plasma calcium increased significantly (5. 5 vs. 7 mg/dl), while PTH mRNA decreased by 40% and VDR mRNA increased by 60%. Neither parathyroid gland weight nor total RNA was significantly affected. When chicks were repleted with l, 25-(OH)2D3, the increase in plasma calcium and VDR mRNA and the decrease in PTH mRNA were considerably more pronounced than those in the absence of the vitamin D source. Furthermore, in the presence of the hormone, parathyroid weight and total RNA decreased significantly with increasing concentrations of dietary calcium. When the chicks were repleted, respectively, with the two levels of l, 25-(OH)2D3, a marked positive interaction was evident between the hormone and dietary calcium in affecting levels of PTH and VDR mRNA. These results suggest that both l, 25-(OH)2D3 and calcium participate in the regulation of PTH and VDR gene transcription in the avian parathyroid gland. Whereas the action of 1, 25-(OH)2D3requires a minimal level of dietary calcium, calcium affects PTH and VDR gene transcription even in the absence of any vitamin D source. © 1993 by The Endocrine Society.
Scientific Publication
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