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Hyperglycemia induces embryopathy, even in the absence of systemic maternal diabetes: an in vivo test of the fuel mediated teratogenesis hypothesis. Reprod Toxicol 2014 Jul;46:129-36

Date

04/12/2014

Pubmed ID

24721120

Pubmed Central ID

PMC4067982

DOI

10.1016/j.reprotox.2014.03.013

Scopus ID

2-s2.0-84899792366   19 Citations

Abstract

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 (25mg/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.

Author List

Baack ML, Wang C, Hu S, Segar JL, Norris AW

Author

Jeffrey L. Segar MD Professor in the Pediatrics department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Diabetes Mellitus, Experimental
Female
Fetal Diseases
Glucose
Hyperglycemia
Organogenesis
Pregnancy
Pregnancy Outcome
Rats
Rats, Sprague-Dawley
Teratogenesis
Tretinoin
jenkins-FCD Prod-486 e3098984f26de787f5ecab75090d0a28e7f4f7c0