PEDIATRICS Vol. 57 No. 5 May 1976, pp. 722-728
This Article
Right arrow Full Text (PDF)
Right arrow P3Rs: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when P3Rs are posted
Right arrow Alert me if a correction is posted
Services
Right arrow E-mail 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 Add to My File Cabinet
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Epstein, M. F.
Right arrow Articles by Chez, R. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Epstein, M. F.
Right arrow Articles by Chez, R. A.

Fetal Lung Lecithin Metabolism in the Glucose-Intolerant Rhesus Monkey Pregnancy

Michael F. Epstein M.D.1, Phillip M. Farrell M.D.1, and Ronald A. Chez M.D.1

1 Pregnancy Research and Neonatal and Pediatric Medicine Branches, National Institute of Child Health and Human Development, Bethesda, Maryland

Fetal lung lecithin metabolism was examined in rhesus monkey gestations complicated by glucose intolerance secondary to maternal streptozotocin (STZ) administration. Fetuses of STZ-treated mothers were delivered at 85% to 89% of term and were compared to two control groups of fetuses from normal pregnancies—one group age-matched to the STZ pregnancies, and the other composed of fetuses delivered in the final 10% of gestation. In the glucose-intolerant pregnancies, two measures of fetal lung lecithin biosynthesis—the amniotic fluid lecithin-to-sphingomyelin (L/S) ratio and the rate of 14C-choline incorporation into lecithin in fetal lung slices—were significantly greater than in age-matched normal gestations and were similar to results in late-gestation controls. However, lung lecithin concentrations in the glucose-intolerant group were comparable to the age-matched controls, and both were significantly less than in the late-gestation controls. Since the gestational age, mode of delivery, and fetal acid-base status were the same in the age-matched groups, we conclude that these changes in fetal lung lecithin metabolism are due to the effects of maternal glucose intolerance.

Submitted on May 10, 1975
Accepted on August 22, 1975




This article has been cited by other articles:


Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
W. Z. Martini, O. Irtun, D. L. Chinkes, R. E. Barrow, and R. R. Wolfe
Glucose effects on lung surfactant kinetics in conscious pigs
Am J Physiol Endocrinol Metab, October 1, 2000; 279(4): E920 - E926.
[Abstract] [Full Text] [PDF]