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Articles in PresS, published online ahead of print March 27, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00046.2002
Submitted on February 4, 2002
Accepted on March 18, 2002
1 Obstetrics and Gynecology, Washington University School of Medicine, St. Louis, MO, USA
2 Obstetrics and Gynecology, Washington University School of Medicine, St. Louis, MO, USA; Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO, USA
* To whom correspondence should be addressed. E-mail: moleyk{at}msnotes.wustl.edu.
Mammalian preimplantation embryos experience a critical switch from an oxidative to a predominantly glycolytic metabolism. In this study, the change in nutrient metabolism, between the 2-cell and blastocyst stage, was followed by measuring single embryo concentrations of tri-carboxylic acid (TCA) cycle and glycolytic metabolites using microfluorometric enzymatic cycling assays. Having established the normal values, further changes that occur as a result of the induction of apoptosis by exposure to high glucose conditions were examined. From a 2-cell to a blastocyst stage, the embryos experienced an increase in TCA metabolites and a dramatic increase in fructose-1,6-phosphate. The high TCA metabolites may result from accumulation of substrate due to a slowing of TCA cycle metabolism as glycolysis predominates. Embryos exposed to elevated glucose conditions experienced significantly lower FBP, suggesting decreased glycolysis, significantly higher pyruvate, suggesting increased pyruvate uptake by the embryos in response to decreased glycolysis, and increased TCA metabolites, suggesting an inability to oxidize the pyruvate and a slowing of the TCA cycle. We speculate that the glycolytic changes lead to dysfunction of the outer mitochondrial membrane that results in the abnormal TCA metabolite pattern and triggers the apoptotic event.
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