作者: Sumant S Chugh , Elisabeth I Wallner , Yashpal S Kanwar
DOI: 10.1053/S0270-9295(03)00136-0
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摘要: Maternal diabetes has an adverse influence on the intrauterine growth of fetus, which is attributable to exposure mammalian embryo abnormal metabolic environment. A sustained fetus such environment (ie, elevated concentration glucose), during first 6 8 weeks gestation in humans may result diabetic embryopathy, characterized by a multitude congenital birth defects, including those nervous, cardiovascular, skeletal, and urogenital systems. The abnormalities be associated with caudal regression syndrome or occur alone form partial total renal agenesis. Similarly, increase incidence morphogenetic defects observed offsprings streptozotocin-induced rats mice also nonobese mice. In certain instances, failure lower part embryos newborn been animals severe state. For further delineation mechanisms involved pathogenesis investigators used whole-embryo culture systems, found that glucose can induce mainly confined body involving genitourinary system. dysmorphogenesis embryonic metanephros when it subjected high concentrations D-glucose its epimer D-mannose. This article discusses aspects embryopathy emphasis changes fetal high-glucose ambience.