1978
DOI: 10.1016/0006-2952(78)90187-9
|View full text |Cite
|
Sign up to set email alerts
|

Acute effect of estradiol on the renal vitamin D hydroxylases in Japanese quail

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

1
15
0

Year Published

1979
1979
2011
2011

Publication Types

Select...
6
2
1

Relationship

1
8

Authors

Journals

citations
Cited by 29 publications
(16 citation statements)
references
References 22 publications
1
15
0
Order By: Relevance
“…However, it was unclear whether the defect recognized represents an altered enzyme response to phosphate depletion alone or is indicative of a generalized regulatory anomaly. Thus, we undertook the work documented in this report to study the modulation of normal and Hyp-mouse renal 1 a-hydroxylase by the other major effector of enzyme activity known in animal species, PTH (27)(28)(29) enhance enzyme activity in Hyp-mice as it does in normal animals, despite a significant reduction of plasma calcium concentration in the mutants (Fig. 1).…”
Section: Resultsmentioning
confidence: 99%
“…However, it was unclear whether the defect recognized represents an altered enzyme response to phosphate depletion alone or is indicative of a generalized regulatory anomaly. Thus, we undertook the work documented in this report to study the modulation of normal and Hyp-mouse renal 1 a-hydroxylase by the other major effector of enzyme activity known in animal species, PTH (27)(28)(29) enhance enzyme activity in Hyp-mice as it does in normal animals, despite a significant reduction of plasma calcium concentration in the mutants (Fig. 1).…”
Section: Resultsmentioning
confidence: 99%
“…Recently we have also reported that estradiol administration in rats increases the tissue content of l,25-(OH)2D3 (Baksi and Kenny, 1978a). Our previous study has shown that estradiol can stimulate 1,25-(OH)2D3 production in Japanese quail within 4 h and that this response occurs prior to the hypercalcemic response of estradiol (Baksi and Kenny, 1978b). A comparable study of the dose-and time-relationship with PTH has not been done to our knowledge.…”
mentioning
confidence: 86%
“…This increase of 1,25(OH) 2 D is independent of a rise in maternal PTH which remains in the low-normal range in the 1 st trimester 43,[66][67][68][69] . Studies have shown that that CYP27B1 activity can be regulated by other sources including parathyroid hormonerelated protein (PTHrP), oestradiol, prolactin (PRL) and placental lactogen [70][71][72] , all of which are increased in pregnancy and which may help explain the rise in 1,25(OH) 2 D independent of PTH responses. Interestingly, 1,25(OH) 2 D does not readily cross the placenta.…”
Section: Vitamin D and The Regulation Of Mineral Homeostasis During Pmentioning
confidence: 99%