Abstract
Diabetic embryopathy is a theoretical enigma and a clinical challenge. Both type 1 and type 2 diabetic pregnancy carry a significant risk for fetal maldevelopment, and the precise reasons for the diabetes-induced teratogenicity are not clearly identified. The experimental work in this field has revealed a partial, however complex, answer to the teratological question, and we will review some of the latest suggestions.
Keywords:
Anomalies; development; diabetes in pregnancy; epigenetics; gene expression; malformations.
MeSH terms
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Animals
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Apoptosis
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Arachidonic Acid / metabolism
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Diabetes Mellitus / diagnosis
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Diabetes Mellitus / therapy
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Diabetes Mellitus, Experimental
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Endoplasmic Reticulum Stress
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Epigenesis, Genetic
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Female
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Fetal Diseases / diagnosis
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Fetal Diseases / therapy
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Genetic Predisposition to Disease
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Glucose / metabolism
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Glycation End Products, Advanced / metabolism
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Hypoxia
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Isoprostanes / chemistry
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Ketones / metabolism
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Mice
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Nitrogen / chemistry
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Oxidative Stress*
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Pregnancy
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Pregnancy in Diabetics / diagnosis*
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Pregnancy in Diabetics / therapy
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Rats
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Reactive Oxygen Species / metabolism
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Receptor for Advanced Glycation End Products / metabolism
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Teratogens / metabolism
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Teratology
Substances
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Ager protein, mouse
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Glycation End Products, Advanced
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Isoprostanes
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Ketones
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Reactive Oxygen Species
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Receptor for Advanced Glycation End Products
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Teratogens
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Arachidonic Acid
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Glucose
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Nitrogen