Insulin-like growth factor I (IGF-I) mediates the majority ofthe growth-promoting effects of growth hormone (GH) after birth.1In the prenatal period, GH does not appear to have a major influenceon fetal growth, whereas IGF-I does. Infants with congenitalGH deficiency and defects in the GH-receptor gene have onlymild retardation of growth at birth,2,3,4 whereas transgenicmice with a homozygous defect of the IGF-I gene (IGF-I knockoutmice) have profound embryonic and postnatal growth retardation.5,6,7Although there is no direct evidence that IGF-I has a prominentrole in human fetal growth, fetal tissues express IGF-I froman early . . . [Full Text of this Article]
Case Report
Methods
Endocrine Studies
Assays
Molecular Studies
Results
Endocrine Studies
Neurologic Studies
Molecular Studies
Discussion
Source Information
From the Departments of Endocrinology (K.A.W., M.O.S.) and Chemical Endocrinology (C.C.-H., A.J.L.C.), St. Bartholomew's Hospital, London.
Address reprint requests to Dr. Clark at the Department of Chemical Endocrinology, 51-53 Bartholomew Close, St. Bartholomew's Hospital, London EC1A 7BE, United Kingdom.
References
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De Benedetti, F., Pignatti, P., Vivarelli, M., Meazza, C., Ciliberto, G., Savino, R., Martini, A.
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