Effects of insulin-like growth factors on chick embryo hepatocytes

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Abstract
Biological effects of insulin-like growth factors (IGF) I and II on primary cultures of chick embryo liver cells were investigated and compared with the biological effect of insulin, and with competitive binding of the 3 hormones to their respective binding sites. IGF I and II stimulate the incorporation of D[U-14C]-glucose into liver cell glycogen in a time- and dose-dependent manner, but with a 5- to 10-fold lower potency than insulin. Both IgF also lead to enhanced incorporation of 5-[3H]uridine and L[U-14C]valine into trichloroacetic acid (TCA) insoluble material and to activation of ornithine decarboxylase activity. Their potency in stimulating RNA synthesis and ornithine decarboxylase activity is comparable to that of insulin. Protein synthesis is maximally stimulated at 3 nM by all 3 hormones. In the competitive binding studies, IGF I and II are 10-fold less potent than insulin in competing for [125I]insulin binding, but 100-fold more potent than insulin in competing for [125I]IGF I or II binding. IGF I and II stimulate the same metabolic indices as insulin in the chick embryo liver. By comparing these biological effects with competitive binding data it appears that IGF act on glucose metabolism in the chick embryo liver via the insulin receptor, whereas stimulation of growth indices by IGF and insulin appears to be mediated by their own specific receptors.

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