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Postnatal growth is dependent on growth hormone (GH). Patients presenting with GH deficiency exhibit growth failure. The molecular defects identified so far as responsible for postnatal growth retardation are alterations in the GH, GH receptor and GH-releasing hormone receptor genes and in the gene of the pituitary transcription factor Pit-1. Even when severe GH deficiency is observed in patients harboring such molecular defects, only mild growth delay is observed at birth. The growth effects of GH in humans are therefore more important after birth, and GH seems to play a minor role during intrauterine development. Insulin-like growth factor-I (IGF-I) mediates most of the effects of GH during the postnatal period. IGF-I acts both as a mitogen and a differentiation factor. Transgenic mice with a targeted disruption of the IGF-I gene exhibit severe intrauterine as well as postnatal growth deficiency (1–3). Furthermore, this mouse has a higher perinatal death rate, delayed
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