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The metabolism of cholecalciferol in Japanese quail, by Saleh Hamad Sedrani.

The metabolism of cholecalciferol in Japanese quail, by Saleh Hamad Sedrani.
The metabolism of cholecalciferol in Japanese quail, by Saleh Hamad Sedrani.

The metabolism of 25 dihyoxycholecalciferol (25 HCC) was studied in Japanese quail in relation to age and to reproductive activity and its regulation by sex hormones and parathyroid hormone alone and in combination was also investigated. This metabolism was studied using kidney homogenates incubated with 311-labelled 25 HCC and the labelled metabolites were separated by thin layer and column chromatography.The results showed that the production of 1,25 dihydroxycholecalciferol (1,25 DHCC) increased and the biosynthesis of 24,25 dihydroxycholecalciferol (24,25 DHCC) decreased in female birds with the approach of sexual maturity. In male birds the production of 1,25 DHCC decreased with age and the activity of 25 HCC-1-hydroxylase was completely suppressed at sexual maturity.Kidneys of birds that were laying regularly produced mainly 1,25 DHCCeven during natural short pauses between clutches or during pauses artificially induced by feeding methallibure, an ovulation inhibitor, whereas in non-laying birds, ones having long natural or artificial pauses between laying sequences, adult males, and immature birds, 24,25 D11CC was the major metabolite. When laying birds were fed on a sulphanilamide-containing diet which inhibited egg shell calcification the activity of 25 HCC-1-hydroxylase in their kidneys was reduced significantly. Injection of parathyroid extract (PTE) into immature birds, adult male, and methallibure or sulphanilamide-fed laying females significantly increased the production of 1,25 DHCC and inhibited the biosynthesis of 24,25 DHCC. These results suggest that ovulation is unlikely to be involved in the stimulation of 1,25 DHCC production and indicate that PTH may be the key factor involved in controlling 1,25 DHCC production in laying birds.Administration of oestrogen to immature birds stimulated the production of 1,25 DHCC and inhibited the biosynthesis of 24,25 DHCC, whereas testosterone inhibited the production of 1,25 DHCC whether given alone or in combination with oestrogen. PTE overcame the inhibition of 1,25 DHCC biosynthesis evoked by testosterone. It is suggested that the presence of PTH is required for oestrogen plus androgen to stimulate the production of 1,25 DHCC to the extent observed in normal laying birds.The increased 25 HCC-1-hydroxylase activity occurring during the reproduction period of female birds may be of physiological significance in increasing the amounts of 1,25 DHCC needed to stimulate the absorption of calcium from the gut and in mobilizing calcium from the medullary bone under the influence of PTH for egg shell formation.

University of Southampton
Sedrani, Saleh Hamad
5d3c5f9b-fef0-41ad-9de3-62db4e7c0b7e
Sedrani, Saleh Hamad
5d3c5f9b-fef0-41ad-9de3-62db4e7c0b7e
Taylor, T. G.
9542b431-59d6-4531-aad0-169c205eedad

Sedrani, Saleh Hamad (1979) The metabolism of cholecalciferol in Japanese quail, by Saleh Hamad Sedrani. University of Southampton, Doctoral Thesis, 140pp.

Record type: Thesis (Doctoral)

Abstract

The metabolism of 25 dihyoxycholecalciferol (25 HCC) was studied in Japanese quail in relation to age and to reproductive activity and its regulation by sex hormones and parathyroid hormone alone and in combination was also investigated. This metabolism was studied using kidney homogenates incubated with 311-labelled 25 HCC and the labelled metabolites were separated by thin layer and column chromatography.The results showed that the production of 1,25 dihydroxycholecalciferol (1,25 DHCC) increased and the biosynthesis of 24,25 dihydroxycholecalciferol (24,25 DHCC) decreased in female birds with the approach of sexual maturity. In male birds the production of 1,25 DHCC decreased with age and the activity of 25 HCC-1-hydroxylase was completely suppressed at sexual maturity.Kidneys of birds that were laying regularly produced mainly 1,25 DHCCeven during natural short pauses between clutches or during pauses artificially induced by feeding methallibure, an ovulation inhibitor, whereas in non-laying birds, ones having long natural or artificial pauses between laying sequences, adult males, and immature birds, 24,25 D11CC was the major metabolite. When laying birds were fed on a sulphanilamide-containing diet which inhibited egg shell calcification the activity of 25 HCC-1-hydroxylase in their kidneys was reduced significantly. Injection of parathyroid extract (PTE) into immature birds, adult male, and methallibure or sulphanilamide-fed laying females significantly increased the production of 1,25 DHCC and inhibited the biosynthesis of 24,25 DHCC. These results suggest that ovulation is unlikely to be involved in the stimulation of 1,25 DHCC production and indicate that PTH may be the key factor involved in controlling 1,25 DHCC production in laying birds.Administration of oestrogen to immature birds stimulated the production of 1,25 DHCC and inhibited the biosynthesis of 24,25 DHCC, whereas testosterone inhibited the production of 1,25 DHCC whether given alone or in combination with oestrogen. PTE overcame the inhibition of 1,25 DHCC biosynthesis evoked by testosterone. It is suggested that the presence of PTH is required for oestrogen plus androgen to stimulate the production of 1,25 DHCC to the extent observed in normal laying birds.The increased 25 HCC-1-hydroxylase activity occurring during the reproduction period of female birds may be of physiological significance in increasing the amounts of 1,25 DHCC needed to stimulate the absorption of calcium from the gut and in mobilizing calcium from the medullary bone under the influence of PTH for egg shell formation.

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Sedrani 1979 Thesis - Version of Record
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Published date: 1979

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Local EPrints ID: 458843
URI: http://eprints.soton.ac.uk/id/eprint/458843
PURE UUID: 38fad6a8-020c-4074-b8ca-2e9c4fddca8e

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Date deposited: 04 Jul 2022 16:56
Last modified: 21 Jun 2024 17:10

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Contributors

Author: Saleh Hamad Sedrani
Thesis advisor: T. G. Taylor

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