Mechanisms of Congenital Malformations in Pregnancies with Pre-existing Diabetes
| Autor: | Mary R. Loeken |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Endocrinology Diabetes and Metabolism Glucose uptake Pregnancy in Diabetics 030209 endocrinology & metabolism Article 03 medical and health sciences Mice 0302 clinical medicine Pregnancy Internal medicine Diabetes mellitus Internal Medicine medicine Animals Humans Neural Tube Defects Fetus biology business.industry Glucose transporter Neural tube Embryo medicine.disease Embryonic stem cell Diabetes Gestational Oxidative Stress 030104 developmental biology medicine.anatomical_structure Endocrinology Hyperglycemia biology.protein GLUT2 Female business |
| Zdroj: | Curr Diab Rep |
| ISSN: | 1539-0829 |
| Popis: | PURPOSE OF REVIEW: Fetuses of diabetic mothers are at increased risk for congenital malformations. Research in recent decades using animal and embryonic stem cell models has revealed many embryonic developmental processes that are disturbed by maternal diabetes. The aim of this review is to give clinicians a better understanding of the reasons for rigorous glycemic control in early pregnancy, and to provide background to guide future research. RECENT FINDINGS: Mouse models of diabetic pregnancy have revealed mechanisms for altered expression of tissue-specific genes that lead to malformations that are more common in diabetic pregnancies, such as neural tube defects (NTDs) and congenital heart defects (CHDs), and how altered gene expression causes apoptosis that leads to malformations. Embryos express the glucose transporter, GLUT2, which confers susceptibility to malformation, due to high rates of glucose uptake during maternal hyperglycemia and subsequent oxidative stress; however, the teleological function of GLUT2 for mammalian embryos may be to transport the amino sugar glucosamine (GlcN) from maternal circulation to be used as substrate for glycosylation reactions and to promote embryo cell growth. Malformations in diabetic pregnancy may be not only due to excess glucose uptake but also due to insufficient GlcN uptake. SUMMARY: Avoiding maternal hyperglycemia during early pregnancy should prevent excess glucose uptake via GLUT2 into embryo cells, and also permit sufficient GLUT2-mediated GlcN uptake. |
| Databáze: | OpenAIRE |
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