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