New concepts in diabetic embryopathy
1Department of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD 21201, USA. zzhao@fpi.umaryland.edu
Insights
Diabetic embryopathy, a cause of birth defects in diabetic pregnancies, persists despite advanced care. Research using animal models highlights cellular and metabolic disruptions, necessitating collaboration for human applications.
Area of Science:
- Reproductive biology
- Developmental toxicology
- Endocrinology
Background:
- Diabetes mellitus contributes to approximately 10% of fetal anomalies in pregnancies affected by the condition.
- Despite advanced perinatal care and glycemic control in developed nations, diabetic pregnancies exhibit elevated birth defect rates compared to the general population.
Purpose of the Study:
- To review the cellular and molecular mechanisms underlying diabetic embryopathy.
- To emphasize the need for translational research bridging animal studies and human clinical applications.
Main Methods:
- Review of animal models investigating diabetic embryopathy.
- Analysis of cellular activities (proliferation, apoptosis) and intracellular metabolic stress (nitrosative, oxidative, endoplasmic reticulum stress).
Main Results:
- Animal models demonstrate that major cellular activities and intracellular metabolic conditions are linked to diabetic embryopathy.
- Key factors include disruptions in proliferation, apoptosis, and various forms of cellular stress.
Conclusions:
- Diabetic embryopathy involves complex cellular and metabolic dysregulation.
- Translating findings from animal models to human clinical practice requires interdisciplinary collaboration among basic, preclinical, and clinical researchers.
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.
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