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of the Insulin-Like Growth Factor I Messenger Ribonucleic Acid Response to Growth Hormone in Rat Hepatocyte Primary Culture1
Unité de Diabétologie et Nutrition, School of Medicine, The University of Louvain, B-1200 Brussels, Belgium
Address all correspondence and requests for reprints to: Jean-Paul Thissen, M.D., Unité de Diabétologie et Nutrition, UCL/DIAB 5474 Avenue Hippocrate, 54, B-1200 Brussels, Belgium. E-mail: thissen{at}diab.ucl.ac.be
The cytokines are the putative mediators of the catabolic reaction that
accompanies infection and trauma. Evidence suggests that their
catabolic actions are indirect and potentially mediated through changes
in hormonal axis such as the hypothalamo-pituitary-adrenal axis.
Insulin-like growth factor I (IGF-I) is a GH-dependent growth factor
that regulates the protein metabolism. To determine whether cytokines
can directly inhibit the production of IGF-I by the liver, we
investigated the regulation of IGF-I gene expression by interleukin
(IL)-1ß, IL-6, and tumor necrosis factor (TNF)-
(10 ng/ml) in a
model of rat primary cultured hepatocytes. Hepatocytes were isolated by
liver collagenase perfusion and cultured on Matrigel 48 h before
experiments. Each experiment was performed in at least three different
animals. In the absence of GH, IL-1ß and TNF- did not affect the
IGF-I messenger RNA (mRNA) basal levels, whereas IL-6 increased it by a
factor of 2.5 after 24 h (P < 0.05). GH (500
ng/ml) alone stimulated the IGF-I gene expression markedly (5- to
10-fold increase) after 24 h (P < 0.001).
IL-1ß, and TNF- to a lesser extent, dramatically inhibited the
IGF-I mRNA response to GH (IL-1ß: -82%, P <
0.001 and TNF-: -47%, P < 0.01). The
half-maximal inhibition of the IGF-I mRNA response to GH was observed
for a concentration of IL-1ß between 0.1 and 1 ng/ml. Moreover,
IL-1ß abolished the IL-6-induced IGF-I mRNA response. In contrast,
IL-6 did not impair the IGF-I mRNA response to GH. To determine the
potential role of the GH receptor (GHR) and the GH-binding protein
(GHBP) in this GH resistance, we assessed the GHR and GHBP mRNAs
response to these cytokines. GH alone did not affect the GHR/GHBP mRNA
levels. IL-1ß markedly decreased the GHR and GHBP mRNA levels
(respectively, -68% and -60%, P < 0.05).
Neither TNF- nor IL-6 affected the GHR/GHBP gene expression. In
conclusion, our results show that IL-1ß, and TNF- to a lesser
extent, blunt the IGF-I mRNA response to GH. The resistance to GH
induced by IL-1ß might be mediated by a decrease of GH receptors, as
suggested by the marked reduction of GHR mRNA. These findings suggest
that decreased circulating IGF-I, in response to infection and trauma,
may be caused by a direct effect of cytokines at the hepatocyte level.
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