The insulin-like growth factors, IGF-I and IGF-II, are important regulators of growth, differentiation and maintenance of differentiated function (Daughaday and Rotwein, 1989), primarily through activation of the IGF-I receptor, a transmembrane tyrosine kinase (Ullrich et al., 1986). In addition to these typical growth factor-like effects, the IGFs, by virtue of their homology to insulin, and the similarity of the insulin and IGF-I receptors, can also elicit insulin-like metabolic effects. The latter effects are presumably the result of “heterologous” activation of the insulin receptor by the IGFs. As described elsewhere in this volume, the bioavailability and action of the IGFs are modulated by a family of IGF-binding proteins.