Autocrine and Paracrine Effects of Insulin-like Growth Factors and Their Binding Proteins
Based on the classical endocrine model of IGF-I to act on target cells after being secreted into the circulation, liver seems to be the organ responsible 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 culture, but it maintains the capacity to stimulating leucine incorporation, an action which mirrors its metabolic effect (Barreca et al. 1992b). Since it is believed that the metabolic effects of IGFs are exerted through the insulin receptors, these data are in agreement with the findings that hepatocytes are devoid of IGF-I receptors (Caro et al. 1988). If the liver is the major producer of IGF-I, the lack of IGF-I mitogenic effect on hepatocytes is a support for the endocrine hypothesis of IGF-I mode of action.
KeywordsGranulosa Cell Follicular Fluid Human Granulosa Cell Stimulate Thymidine Incorporation Fetal Mouse Fibroblast
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