New concepts in diabetic embryopathy

Abstract

Diabetes mellitus is responsible for nearly 10% of fetal anomalies in diabetic pregnancies. Although aggressive perinatal care and glycemic control are available in developed countries, the birth defect rate in diabetic pregnancies remains higher than that in the general population. Major cellular activities (ie, proliferation and apoptosis) and intracellular metabolic conditions (ie, nitrosative, oxidative, and endoplasmic reticulum stress) have been shown to be associated with diabetic embryopathy using animal models. Translating advances made in animal studies into clinical applications in humans requires collaborative efforts across the basic research, preclinical, and clinical communities.