Am J Physiol Cell Physiol AJP: Cell Physiology
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Am J Physiol Cell Physiol 279: C1906-C1917, 2000;
0363-6143/00 $5.00
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Vol. 279, Issue 6, C1906-C1917, December 2000

Inhibition of growth hormone action in models of inflammation

Pearl L. Bergad1, Sarah Jane Schwarzenberg1, Jeffrey T. Humbert1, Michelle Morrison1, Sherani Amarasinghe2, Howard C. Towle2, and Susan A. Berry1,3

Departments of 1 Pediatrics, 2 Biochemistry, Molecular Biology and Biophysics, and the 3 Institute of Human Genetics, University of Minnesota, Minneapolis, Minnesota 55455

Growth hormone (GH) action is attenuated during the hepatic acute-phase response (APR). To understand this attenuation, we asked whether GH and cytokine-signaling pathways intersect during an APR. In hypophysectomized rats treated with lipopolysaccharide (LPS), accumulation of activated signal transducer and transcription activator 5 (Stat5) in hepatic nuclei in response to GH and its binding to a GH response element (GHRE) from the serine protease inhibitor (Spi) 2.1 promoter are diminished in a time-dependent manner. Similarly, accumulation of activated Stat3 in hepatic nuclei in response to LPS and its binding to a high-affinity sis-inducible element (SIE) are also diminished by the simultaneous administration of GH. In functional assays with primary hepatocytes, LPS-stimulated monocyte-conditioned medium (MoCM) inhibits the GH response of Stat5-dependent Spi 2.1 reporter activity but induces Stat3-dependent Spi 2.2 reporter activity, as in an APR. Similar results are obtained when hepatocytes are treated with either tumor necrosis factor-alpha (TNF-alpha ) or interleukin (IL)-1beta . TNF-alpha , IL-1beta , and IL-6 also inhibit GH-induced Spi 2.1 mRNA expression in hepatocytes. Thus inhibition of the GH signaling pathway during an APR results in reduced expression of GH-responsive genes.

signal transducers and activators of transcription proteins; rat liver; serine protease inhibitors 2.1 and 2.2; lipopolysaccharide


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