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Tissue Expression of Insulin-like Growth Factor Ie growth factors (IGFs) which are subsequently released into the bloodstream to exert anabolic effects on peripheral tissues such as cartilage and skeletal muscle. During the last decade, our knowledge and understanding of the mechanism of action of somatomedins have undergone dramatic changes. It i

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Insulin-like Growth Factor Binding Proteins: Biochemical Characterizationtructurally distinct binding proteins (IGFBPs; Drop et al. 1992). These proteins bind IGF-1 and IGF-II with varying affinities in the range 10.-10.1/mol two of them, IGFBP-2 and IGFBP-6, have a strong preferential affinity for IGF-II, whereas none appears to show a marked preference for IGF-I. An in

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Role of Insulin-like Growth Factor Binding Proteins in Modulating Insulin-like Growth Factor Actionructurally distinct forms of IGF binding proteins have been cloned and their cDNA sequences determined (Shimasaki et al. 1991). Although all six share structural homology many of their features appear to be distinct. Structural characterization and purification of these proteins has made it possible

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Autocrine and Paracrine Effects of Insulin-like Growth Factors and Their Binding Proteinsble for such mode of action. A support for this hypothesis is that liver accounts for most of the circulating IGF-I (Schwander et al. 1983) and that it is insensitive to its action. At variance with EGF, IGF-I is unable to stimulate thymidine incorporation on isolated adult rat hepatocytes in cultur

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Use of Transgenic and Genetic Models to Study the Neuroendocrine Regulation of Growth Hormone Secretimals and after destruction or removal of key components of the hypothalamic-GH-IGF-I axis have given considerable insight into the individual components, the ablative procedures all give rise to other neuronal and/or hormonal deficiencies that complicate interpretation of the results. The recent av

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Biosynthesis and Biological Role of Insulin-like Growth Factors in the Nervous Systemrapid proliferation of the stem cells, migration and differentiation into neurones and glia, and the establishment of synaptic connections as well as the selective death of specific cells. Disturbance in this growth process can often result in permanent and irreversible defects in CNS structure and

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Mechanisms of Intrauterine Growth Retardation: Role of Fetal and Maternal Hormones perinatal morbidity and mortality. Fetuses with IUGR are more likely to be stillborn or die in the neonatal period. Neonates with IUGR have greater risk of asphyxia induced encephalopathy with the consequent risks of neurological dysfunction. Infants who are born small may either show catchup growt