Attenuated Insulin Release and Storage in Fetal Sheep Pancreatic Islets with Intrauterine Growth Restriction

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These data show that insulin synthesis is a major limitation in IUGR fetal islets and begins to explain the significant reduction in glucose-stimulated insulin secretion in the IUGR fetus. An inability to properly respond to glucose and increase oxidative metabolism may be, at least partially responsible for the impaired insulin secretion. However, greater fractional insulin secretion indicates potential modifications in beta-cells to respond to these limitations.

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