Our lack of basic knowledge about the basic mechanisms of transitional hypoglycemia and other forms of hypoglycemia in newborns underlies the ongoing controversies over standards for managing these conditions. To… Click to show full abstract
Our lack of basic knowledge about the basic mechanisms of transitional hypoglycemia and other forms of hypoglycemia in newborns underlies the ongoing controversies over standards for managing these conditions. To address this deficiency, the authors evaluated regulation of insulin secretion in fetal, newborn, and adult rats. The results demonstrate that transitional hypoglycemia in normal neonates and persistent hypoglycemia in high-risk infants both reflect altered beta-cell insulin regulation. These findings provide a new foundation for improving detection and management and preventing hypoglycemic brain injury in normal neonates and, especially, in infants with persistent hypoglycemia and genetic forms of congenital hyperinsulinism.
               
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