Central and peripheral actions of somatostatin on the growth hormone–IGF-I axis
J. Clin. Invest. Robert D. Murray, et al. 114:349 doi:10.1172/JCI19933 [Go to this article.]

Figure 2
SRIF suppresses GH-induced hepatocyte IGF-I. (A) Isolated rat hepatocytes were incubated with GH (100 or 500 ng/ml) for 24 hours with or without 1 hour preincubation with 100 nM SRIF or octreotide (OCT). RNA was quantitated by RPA analysis. Upper panel: representative blot. Lower panel: mean fold induction of IGF-I mRNA of three individual experiments after normalization for β-actin. *P < 0.05 compared with GH-treated cells. (B) Representative RPA quantitation for IGF-I and β-actin content of isolated rat hepatocytes following incubation with 100 nM SRIF or octreotide for 24 hours with no GH stimulation. Upper panel: IGF-I; lower panel: β-actin. (C) RPA analysis of IGF-I and β-actin from isolated rat hepatocytes treated with GH (500 ng/ml) for 24 hours with and without preincubation with 0.01–100 nM SRIF (upper two panels), or 0.1–500 nM octreotide for 1 hour (lower two panels).