Although neither GH nor T4 appears to be an important determinant of fetal growth, insulin may act as a growth-promoting hormone during the fetal period. Infants born of diabetic mothers are often larger than normal, especially when the diabetes is poorly controlled. Because glucose readily crosses the placenta, high concentrations of glucose in maternal blood increase fetal blood glucose and stimulate the fetal pancreas to secrete insulin. In the rare cases of congenital deficiency of insulin that have been reported, fetal size is below normal. Structurally, insulin is closely related to IGF-I and IGF-II and, when present in adequate concentrations, can react with IGF-I receptors, which are closely related structurally to the insulin receptor. We do not know if the effects of insulin on fetal growth are mediated by the insulin receptor or IGF-I receptors.
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