Hyperglycemia induces embryopathy, even in the absence of systemic maternal diabetes: An in vivo test of the fuel mediated teratogenesis hypothesis

Michelle L. Baack, Chunlin Wang, Shanming Hu, Jeffrey L. Segar, Andrew W. Norris

Research output: Contribution to journalArticle

17 Scopus citations


Embryonic exposure to excess circulating fuels is proposed to underlie diabetic embryopathy. To isolate the effects of hyperglycemia from the many systemic anomalies of diabetes, we infused 4. mg/min glucose into the left uterine artery of non-diabetic pregnant rats on gestation days (GD) 7-9. Right-sided embryos and dams exhibited no glucose elevation. Embryos were assessed on GD13, comparing the left versus right uterine horns. Hyperglycemic exposure increased rates of embryopathy, resorptions, and worsened embryopathy severity. By contrast, saline infusion did not affect any of these parameters. To assess for possible embryopathy susceptibility bias between uterine horns, separate dams were given retinoic acid (25. mg/kg, a mildly embryopathic dose) systemically on GD7.5. The resultant embryopathy rates were equivalent between uterine horns. We conclude that hyperglycemia, even in the absence of systemic maternal diabetes, is sufficient to produce in vivo embryopathy during organogenesis.

Original languageEnglish (US)
Pages (from-to)129-136
Number of pages8
JournalReproductive Toxicology
Publication statusPublished - Jul 2014



  • Animal model
  • Diabetes
  • Embryopathy
  • Fuel-mediated teratogenesis
  • Hyperglycemia
  • Teratogenesis

ASJC Scopus subject areas

  • Toxicology

Cite this