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There is evidence that the hormonal control of hepatic IGF-I production is mediated by GH and insulin. To elucidate the role of these hormones further we administered s.c. or i.p. insulin (at 2·5 and 5·0 IU/day) and/or GH (0·8 IU/day) to rats made diabetic with streptozotocin 16 days previously. Hepatic IGF-I production was then assessed by quantifying hepatic IGF-I mRNA levels by autoradiography of Northern blots. Diabetes resulted in a fivefold reduction in hepatic IGF-I mRNA levels (optical density (OD) of the 0·7–1·1 kb band: controls, 1·3±0·09; diabetics, 0·28±0·08; P<0·01), which was not significantly changed by treatment with s.c. insulin (OD: low dose, 0·55±0·05; high dose, 0·58±0·05) or low dose i.p. insulin (OD: 0·40±0·03). High dose i.p. insulin enhanced hepatic IGF-I mRNA levels (OD: 0·93±0·23) compared with diabetic rats (P<0·01) and those given high dose s.c. insulin (P<0·04), despite the blood glucose values being similar in the treated groups (i.p., 4·72±0·29 mmol/l; s.c., 3·32±0·03 mmol/l). Administration of GH alone partially restored the hepatic IGF-I mRNA level (OD: GH-treated, 1·00±0·05; diabetic, 0·28±0·08; P<0·01), whilst having no effect on blood glucose values (diabetic, 36·35±0·45 mmol/l; GH-treated, 38·65±2·39 mmol/l). Additional administration of s.c. insulin completely restored IGF-I mRNA levels to those of controls (OD: low dose, 1·35±0·14; high dose, 1·27 ± 0·18). These observations indicate that insulin and GH are required for full expression of hepatic IGF-I mRNA and that insulin given i.p. is more potent than that given s.c. at stimulating hepatic synthesis of IGF-I.