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פותח על ידי קלירמאש פתרונות בע"מ -
Modulation of chick intestinal and renal calbindin gene expression by dietary vitamin D3, 1,25-dihydroxyvitamin D3, calcium and phosphorus
Year:
1990
Authors :
בר, אריה
;
.
שני, משה
;
.
Volume :
72
Co-Authors:
Bar, A., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan, Israel
Shani, M., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan, Israel
Fullmer, C.S., Veterinary College, Cornell University, Ithaca, NY, United States
Brindak, M.E., Veterinary College, Cornell University, Ithaca, NY, United States
Striem, S., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan, Israel
Facilitators :
From page:
23
To page:
31
(
Total pages:
9
)
Abstract:
Synthetic oligonucleotide probes complementary to chick calbindin-28 kDa-mRNA were used to study the latter's regulation and relationship to calbindin in the chick. The effects of vitamin D3 sources and dietary alteration on the genomic expression were characterized by Northern blot and solution hybridization. Intestinal calbindin and its mRNA were almost absent in vitamin D-deficient chicks and were not affected by dietary alteration. Renal calbindin and its mRNA were lower in the vitamin D-deficient than in vitamin D3- or 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)-fed chicks. In the same animal, renal calbindin mRNA and calbindin were higher than intestinal. In vitamin D3-fed chicks, dietary calcium (Ca) or phosphorus (P) restriction induced, and high dietary Ca inhibited, intestinal calbindin and its mRNA synthesis. In the same chicks, dietary P restriction induced renal calbindin mRNA and calbindin synthesis. In 1,25-(OH)2D3-fed chicks, dietary P restriction induced and high dietary Ca inhibited the synthesis of intestinal and renal calbindin. The results suggest that: (a) most of the changes in renal and intestinal calbindin could be attributed to the changes in the mRNA; (b) the adaptation to dietary Ca and P alterations requires vitamin D metabolites; (c) high dietary Ca affects intestinal and renal calbindin-mRNA and calbindin via mechanisms independent of kidney 1-hydroxylase; and (d) plasma Ca and renal calbindin or its mRNA tend to change together in vitamin D-deficient or vitamin D3-fed, but not in 1,25(OH)2D3-fed chicks. © 1990.
Note:
Related Files :
(Kidney)
Animal
animal cell
calcitriol
Chickens
gene expression
Intestines
Kidney
Oligonucleotide Probes
RNA, Messenger
עוד תגיות
תוכן קשור
More details
DOI :
10.1016/0303-7207(90)90236-2
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
20730
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:38
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Scientific Publication
Modulation of chick intestinal and renal calbindin gene expression by dietary vitamin D3, 1,25-dihydroxyvitamin D3, calcium and phosphorus
72
Bar, A., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan, Israel
Shani, M., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan, Israel
Fullmer, C.S., Veterinary College, Cornell University, Ithaca, NY, United States
Brindak, M.E., Veterinary College, Cornell University, Ithaca, NY, United States
Striem, S., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan, Israel
Modulation of chick intestinal and renal calbindin gene expression by dietary vitamin D3, 1,25-dihydroxyvitamin D3, calcium and phosphorus
Synthetic oligonucleotide probes complementary to chick calbindin-28 kDa-mRNA were used to study the latter's regulation and relationship to calbindin in the chick. The effects of vitamin D3 sources and dietary alteration on the genomic expression were characterized by Northern blot and solution hybridization. Intestinal calbindin and its mRNA were almost absent in vitamin D-deficient chicks and were not affected by dietary alteration. Renal calbindin and its mRNA were lower in the vitamin D-deficient than in vitamin D3- or 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)-fed chicks. In the same animal, renal calbindin mRNA and calbindin were higher than intestinal. In vitamin D3-fed chicks, dietary calcium (Ca) or phosphorus (P) restriction induced, and high dietary Ca inhibited, intestinal calbindin and its mRNA synthesis. In the same chicks, dietary P restriction induced renal calbindin mRNA and calbindin synthesis. In 1,25-(OH)2D3-fed chicks, dietary P restriction induced and high dietary Ca inhibited the synthesis of intestinal and renal calbindin. The results suggest that: (a) most of the changes in renal and intestinal calbindin could be attributed to the changes in the mRNA; (b) the adaptation to dietary Ca and P alterations requires vitamin D metabolites; (c) high dietary Ca affects intestinal and renal calbindin-mRNA and calbindin via mechanisms independent of kidney 1-hydroxylase; and (d) plasma Ca and renal calbindin or its mRNA tend to change together in vitamin D-deficient or vitamin D3-fed, but not in 1,25(OH)2D3-fed chicks. © 1990.
Scientific Publication
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