Insulin-like growth factor I (IGF-I) is one of the insulin family of peptides with both metabolic and growth-promoting properties. Liver is the major source of IGF-I, but adult rat liver contains very few, if any, specific binding sites for IGF-I. Fetal rat liver, regenerating liver after partial hepatectomy, and the rat hepatoma cell line HEP-G2, on the other hand, all contain substantial levels of specific IGF-I receptor. Thus, there is a correlation between the proliferative capacity of the cells and their ability to respond in an autocrine manner to an IGF-I stimulus. At the molecular level, the point of regulation of this change in ability to respond to an IGF-I stimulus is not known. One possibility is a change in the transcription of the IGF-I and IGF-I receptor genes, resulting in increased or decreased expression of these proteins. This possibility will be investigated by determining the amount of mRNA for IGF-I and its receptor present in normal adult rat liver, in fetal rat liver, and in regenerating liver after partial hepatectomy. Since there are several different species of mRNA for both IGF-I and its receptor, a solution hybridization/nuclease protection method that permits determination of message type as well as amount will be used. In addition, nuclear run-off transcription will be used to determine if the alterations in message level are due to changes in the rate of transcription of the mRNA's. These techniques of mRNA quantitation will ultimately be used to examine the role of IGF-I and its receptor in liver and other tissues of patients with diabetes, to better understand the function of the insulin-like growth factors in normal and diabetic individuals.