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Unité de Diabétologie et Nutrition, School of Medicine, The University of Louvain, B-1200 Brussels, Belgium
Sepsis induces a state of growth hormone (GH)
resistance associated with a decrease of circulating insulin-like
growth factor (IGF) I, a GH-dependent anabolic hormone mainly produced
by the liver. To address the mechanisms that might trigger GH
insensitivity in sepsis, we investigated the regulation of liver GH
receptor (GHR) and its gene expression by endotoxin.
Endotoxin injection in rats decreased serum IGF-I and liver GH-binding
sites after 10 h. In contrast to liver GHR, circulating GH-binding
protein (GHBP) levels were not significantly reduced after endotoxin
injection. The parallel decrease in IGF-I and GHR and in their
corresponding liver mRNAs suggests that decreased serum IGF-I and liver
GHR were likely to result from decreased liver synthesis. Although GH
administration in control animals significantly enhanced serum IGF-I,
it did fail to prevent the decline in serum IGF-I and liver GH-binding
sites in endotoxemic rats. In this study, we showed that endotoxin
injection induces a state of GH insensitivity associated with decreased
liver GHR. This decline in GHR, which cannot be prevented by exogenous
GH, might contribute to the GH insensitivity observed in sepsis.
growth hormone resistance; insulin-like growth factor I; gene expression
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