description) The timing of and mechanism by which early exposure to uncontrolled diabetes causes abnormalities during preimplantation phase remain to be discovered. The study proposed will attempt to show that the maternal diabetic state initiates a dely in development between ovulation and the 1-cell stage immediately following fertilization. To prove this hypothesis, embryos will be removed at three different stages (a) metaphase II-arrested ooctes, (b) 1-cell embryo, or (c) 2-cell embryo. Oocytes are fertilized in vitro and all embryos are transferred into either diabetic or non-diabetic mice. All embryos will be recovered 48-72 hours later and developmental stages reached by the embryos will be examined. The second portion of this study will attempt to explore the hypothesis that glutathione (GSH) depletion due to oxidative stress is related to the developmental delay. To test this hypothesis, glutathione levels and the activities of three enzymes involved in glutathione-related scavenging will be measured.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Small Research Grants (R03)
Project #
5R03HD034693-02
Application #
2403630
Study Section
Maternal and Child Health Research Committee (HDMC)
Project Start
1996-07-15
Project End
1999-06-30
Budget Start
1997-07-01
Budget End
1999-06-30
Support Year
2
Fiscal Year
1997
Total Cost
Indirect Cost
Name
Washington University
Department
Obstetrics & Gynecology
Type
Schools of Medicine
DUNS #
062761671
City
Saint Louis
State
MO
Country
United States
Zip Code
63130
Carayannopoulos, M O; Chi, M M; Cui, Y et al. (2000) GLUT8 is a glucose transporter responsible for insulin-stimulated glucose uptake in the blastocyst. Proc Natl Acad Sci U S A 97:7313-8
Chi, M M; Pingsterhaus, J; Carayannopoulos, M et al. (2000) Decreased glucose transporter expression triggers BAX-dependent apoptosis in the murine blastocyst. J Biol Chem 275:40252-7