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Our perception of insulin-like growth factor-I (IGF-I) as a growth promoter stems from the original proposal of Salmon & Daughaday (1957) that it mediates the biological actions of pituitary growth hormone (GH). The primary target for GH, it was proposed, is the liver which is stimulated to synthesize IGF-I. The resultant increase in circulating levels of IGF-I promotes cell division and constitutes a major component of the growth response. There is a large body of evidence which relates serum IGF-I concentrations to growth rates; moreover, the liver is the major source of the hormone since it has the highest tissue level of IGF-I mRNA (Murphy et al. 1987) and its synthesis of IGF-I peptide can account, in theory, for the known turnover of IGF-I in the circulation (Schwander et al. 1983).
Subsequently it was shown that IGFs are synthesized to varying degrees in many other tissues. While these observations indicate
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