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 6
SRIF suppression of hepatic IGF-I does not require new protein induction. (A) Isolated primary hepatocytes were pretreated with vehicle or pertussis toxin (PTX, 100 ng/ml) for 24 hours; vehicle, 100 nM SRIF, or octreotide were added; and the cells stimulated with GH (500 ng/ml) one hour later. Cells were incubated for an additional 20 hours and cells harvested. RNA was analyzed for IGF-I content by RPA and loading normalized by β-actin quantitation. The upper panel shows a representative blot, and the lower panel shows mean fold induction of IGF-I mRNA after normalization for β-actin. (B) Primary hepatocytes were pretreated with vehicle or cycloheximide (CHX, 10 μg/ml) for 2 hours and vehicle, 100 nM SRIF, or octreotide for 1 hour before stimulation with GH (500 ng/ml). Cells were incubated for an additional 6 hours and harvested. RNA was analyzed for IGF-I content by RPA and loading normalized by quantitation of β-actin. (C) Primary hepatocytes were treated as for B and IGF-I RNA content quantitated by real-time PCR and normalized for β-actin.