Abstract
Macrosomic infants of diabetic mothers are the result of an early growth delay and an augmented growth towards term. Early growth delay appears to be associated with the increased malformations of these infants. In rat pregnancy diabetes produces with no exception small fetuses. The response of fetal cells to different growth factors has been poorly defined. Therefore 48 h post conception 65 mg/kg streptozotocin i.v, were injected and on day 20 5μCi 3-H thyraidine i.p.. On day 21 after a 14 h fast fetuses were delivered and blood glucose (mg/dl), body weight (g), length (cm) and thymidine incorporation (cpm/mg rib cartilage) were determined: M ± SEM; (n).
Colony formation from isolated chondrocytes of hyperglycemic fetuses in response to pro-/insulin (62.5-250 ng/ml) or IGF I / IGF II (6.25-25 ng/ml) was significantly less (<0.05-0.001) compared to normal fetuses. This demonstrates a defect at the cellular level. Possibly, early growth delay in human diabetes may be explained by a similar mechanism.
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Heinze, E., Vetter, U. FETAL GROWTH IN DIABETIC RAT PREGNANCY - IN VIVO AND IN VITRO STUDIES. Pediatr Res 20, 1193 (1986). https://doi.org/10.1203/00006450-198611000-00116
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DOI: https://doi.org/10.1203/00006450-198611000-00116