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Effects of maternal diabetes on fetal development in rats

The mechanisms underlying the high incidence of fetal abnormalities including fetal lung immaturity during maternal diabetes are not fully understood. Utilizing streptozotocin-diabetic rats as the model, I have examined the role of fetal hyperglycemia and hyperinsulinemia and other factors on fetal adrenal and lung functions in culture. Insulin and glucose did not alter fetal adrenal and lung cell proliferation and adrenal corticosterone output. On the other hand, a novel protein-bound, low molecular weight non-proteinaceous cytotoxic factor was detected in the serum of diabetic animals. In addition, a novel protein with cytostatic activity was found in fetal lungs, the concentration of which increased during diabetes. Partial amino acid sequence and Western Blot analysis revealed this protein to be similar to histone H2B. An extra-nuclear role is suggested for this protein because it appears to be present in the microsomal fraction of fetal lungs. It is concluded that fetal lung immaturity during diabetes may be contributed by cytotoxic and cytostatic factors contained in the serum and fetal lungs, respectively.

Identiferoai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.39344
Date January 1992
CreatorsConliffe, Phyllis R. (Phyllis Rowena)
PublisherMcGill University
Source SetsLibrary and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada
LanguageEnglish
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation
Formatapplication/pdf
CoverageDoctor of Philosophy (Department of Physiology.)
RightsAll items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated.
Relationalephsysno: 001276947, proquestno: NN74892, Theses scanned by UMI/ProQuest.

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