help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Logue, F. C.
Right arrow Articles by Beastall, G. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Logue, F. C.
Right arrow Articles by Beastall, G. H.

Journal of Clinical Endocrinology & Metabolism, Vol 75, 25-29, Copyright © 1992 by Endocrine Society

ARTICLES

Sleep shift dissociates the nocturnal peaks of parathyroid hormone (1- 84), nephrogenous cyclic adenosine monophosphate, and prolactin in normal men

FC Logue, WD Fraser, DS O'Reilly, J Christie, DA Cameron, DC Wallace and GH Beastall
Institute of Biochemistry, Royal Infirmary, Glasgow, Scotland.

The secretion of PTH(1-84) and PRL over a 24-h period in normal subjects has been shown to be highly correlated, with changes in PRL occurring approximately 2 h after those in PTH(1-84). It has been postulated that there may be neuroendocrine control common to PTH(1-84) and PRL. As the secretion of PRL is known to be strongly influenced by sleep we investigated the effect of a 7-h acute sleep shift on the nocturnal secretion of PTH(1-84), PRL, and nephrogenous cAMP, a marker of PTH(1-84) bioactivity. Six normal male subjects were studied on two occasions (study A sleep, 0100-0800 h; study B, 0800-1400 h) with samples withdrawn at 30-min intervals. Sleep shift produced the expected shift in PRL secretion to new time of sleep. The overall timing of the PTH(1-84) nocturnal peak (0200-0600 h) was not altered by sleep shift. However, the start of the rise in PTH(1-84) (0200-0300 h) was blunted (P less than 0.05), and the peak of nephrogenous cAMP, coincident with the nocturnal rise in PTH(1-84) in study A, was markedly attenuated (P less than 0.01). Thus whereas the results of this study argue against a direct neuroendocrine link between PTH(1-84) and PRL, it is postulated that sleep shift disrupts a high degree of temporal organization which, under normal conditions, may allow concerted metabolic effects between PTH(1-84) and other hormones over a 24-h period.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
C. E. Hotchkiss and C. P. Jerome
Evaluation of a nonhuman primate model to study circadian rhythms of calcium metabolism
Am J Physiol Regulatory Integrative Comp Physiol, August 1, 1998; 275(2): R494 - R501.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
G. E.-H. Fuleihan, E. B. Klerman, E. N. Brown, Y. Choe, E. M. Brown, and C. A. Czeisler
The Parathyroid Hormone Circadian Rhythm Is Truly Endogenous--A General Clinical Research Center Study
J. Clin. Endocrinol. Metab., January 1, 1997; 82(1): 281 - 286.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1992 by The Endocrine Society