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Decreased glucose transporter expression triggers BAX-dependent apoptosis in the murine blastocyst

M M Chi1, J Pingsterhaus, M Carayannopoulos

  • 1Departments of Obstetrics/Gynecology and Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

The Journal of Biological Chemistry
|September 21, 2000
PubMed

Insights

High glucose levels reduce glucose transporter (GLUT1) function, triggering apoptosis in mouse blastocysts. This cell death pathway, dependent on BAX, is linked to pregnancy complications in diabetic women.

Area of Science:

  • Reproductive biology
  • Developmental biology
  • Metabolic disorders

Background:

  • Maternal hyperglycemia is a risk factor for adverse pregnancy outcomes, including resorption and malformation.
  • The precise mechanisms by which hyperglycemia affects early embryonic development remain incompletely understood.
  • Glucose transporters play a critical role in nutrient supply to the developing embryo.

Purpose of the Study:

  • To investigate the role of facilitative glucose transporter 1 (GLUT1) in hyperglycemia-induced apoptosis in murine blastocysts.
  • To elucidate the involvement of the BAX-dependent apoptotic pathway in this process.
  • To correlate blastocyst apoptosis with adverse pregnancy outcomes.

Main Methods:

  • Inhibition of GLUT1 expression using high glucose conditions and antisense oligodeoxynucleotides in murine blastocysts.
  • Assessment of GLUT1 protein expression and glucose transport function.
  • Quantification of apoptosis in blastocysts from wild-type and Bax-deficient diabetic mice.
  • Evaluation of pregnancy outcomes (resorptions, malformations) in offspring.

Main Results:

  • Reduced GLUT1 expression and glucose transport significantly increased blastocyst apoptosis.
  • Inhibition of GLUT1 by high glucose or antisense oligonucleotides triggered apoptosis.
  • Blastocysts from diabetic Bax-deficient mice showed reduced apoptosis compared to hyperglycemic wild-type controls, despite decreased glucose transport.
  • Reduced preimplantation apoptosis in Bax-deficient mice correlated with fewer resorptions and malformations.

Conclusions:

  • Hyperglycemia-induced decrease in glucose transport acts as a cell death signal, initiating a BAX-dependent apoptotic cascade in murine blastocysts.
  • Increased blastocyst apoptosis due to maternal hyperglycemia may lead to the loss of essential progenitor cells, contributing to resorption and malformation.
  • These findings highlight a potential mechanism linking maternal diabetes to adverse pregnancy outcomes and suggest therapeutic targets for mitigating these risks.

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