AJP - Endo Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Endocrinol Metab 265: E572-E577, 1993;
0193-1849/93 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Caufriez, A.
Right arrow Articles by Copinschi, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Caufriez, A.
Right arrow Articles by Copinschi, G.

AJP - Endocrinology and Metabolism, Vol 265, Issue 4 E572-E577, Copyright © 1993 by American Physiological Society


ARTICLES

Regulation of maternal IGF-I by placental GH in normal and abnormal human pregnancies

A. Caufriez, F. Frankenne, G. Hennen and G. Copinschi
Department of Obstetrics and Gynecology, Universite Libre de Bruxelles, Belgium.

Throughout gestation, maternal insulin-like growth factor I (IGF-I) increases progressively despite suppressed pituitary growth hormone (GH) secretion. We have previously shown that in normal pregnancy, a specific placental GH variant, rather than human placental lactogen (hPL), substitutes for pituitary GH in the regulation of maternal IGF-I. We studied the maternal IGF-I secretion in a cohort of 286 normal and abnormal pregnancies (617 blood samples). Regardless of pathology and gestational age, IGF-I values correlated with corresponding placental GH but not with hPL values. Similar correlations were evidenced for each 2-wk gestational period between 32 and 39 wk. In pathological pregnancies, when only those hormonal results that are obtained before any treatment are considered and diabetes is excluded, IGF-I levels were closely related to corresponding placental GH, but not to hPL. In women with a fetoplacental unit disorder, low placental GH levels resulted in low IGF-I and in a secondary pituitary GH increase, whereas in patients without detectable impairment of the fetoplacental unit normal placental GH corresponded to normal IGF-I. These results suggest that in pathological as well as in normal pregnancy, placental GH, and not hPL, substitutes for pituitary GH to regulate the maternal IGF-I secretion.


This article has been cited by other articles:


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
F. H. Bloomfield, M. K. Bauer, P. L. Van Zijl, P. D. Gluckman, and J. E. Harding
Amniotic IGF-I supplements improve gut growth but reduce circulating IGF-I in growth-restricted fetal sheep
Am J Physiol Endocrinol Metab, February 1, 2002; 282(2): E259 - E269.
[Abstract] [Full Text] [PDF]


Home page
Mol Hum ReprodHome page
S. Sheikh, P. Satoskar, and D. Bhartiya
Expression of insulin-like growth factor-I and placental growth hormone mRNA in placentae: a comparison between normal and intrauterine growth retardation pregnancies
Mol. Hum. Reprod., March 1, 2001; 7(3): 287 - 292.
[Abstract] [Full Text] [PDF]


Home page
Mol Hum ReprodHome page
K. Englund, B. Lindblom, K. Carlstrom, I. Gustavsson, P. Sjoblom, and A. Blanck
Gene expression and tissue concentrations of IGF-I in human myometrium and fibroids under different hormonal conditions
Mol. Hum. Reprod., October 1, 2000; 6(10): 915 - 920.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online