Differential role of glucocorticoids in mediating endotoxin-induced changes in IGF-I and IGFBP-1

Yue Hua Li, Jie Fan, Charles H. Lang

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

The purpose of the present study as to determine whether endogenous elevations in glucocorticoids mediate the changes in insulin-like growth factor (IGF) I and IGF binding protein (IGFBP) 1 levels in plasma and tissues observed after in vivo administration of lipopolysachcaride (LPS). In overnight-fasted male rats LPS injected via the tail vein decreased the IGF-I concentration in plasma, liver, and skeletal muscle (30-45%) and increased IGF-I content in kidney (~3-fold). LPS also decreased IGF-I mRNA abundance in liver and muscle and increased gene expression in kidney. Concomitantly, IGFBP-1 levels in plasma, liver, and muscle were markedly elevated by LPS. All these changes were associated with a greater than fourfold elevation in plasma corticosterone. Pretreatment of rats with the glucocorticoid receptor antagonist RU-486 completely prevented or blunted the LPS-induced changes in IGF-I content in plasma, liver, muscle, and kidney. In liver and muscle RU-486 significantly attenuated the reduction in IGF-I mRNA abundance produced by LPS, but in kidney the LPS-induced increase in IGF-I mRNA was still evident. In contrast, pretreatment with RU-486 did not prevent or attenuate the LPS-induced increase in IGFBP-1 levels in plasma, liver, or muscle. These data suggest that glucocorticoids play a major role in regulating IGF-I mRNA and peptide content in tissues in response to LPS, but the increased IGFBP-1 in blood and tissues induced by LPS appears largely glucocorticoid independent.

Original languageEnglish (US)
Pages (from-to)R1990-R1997
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume272
Issue number6 41-6
StatePublished - Aug 2 1997

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Insulin-Like Growth Factor Binding Protein 1
Insulin-Like Growth Factor Binding Proteins
Insulin-Like Growth Factor I
Endotoxins
Glucocorticoids
Mifepristone
Liver
Muscles
Kidney
Messenger RNA
Glucocorticoid Receptors
Corticosterone
Tail
Veins
Skeletal Muscle
Gene Expression
Peptides

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

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title = "Differential role of glucocorticoids in mediating endotoxin-induced changes in IGF-I and IGFBP-1",
abstract = "The purpose of the present study as to determine whether endogenous elevations in glucocorticoids mediate the changes in insulin-like growth factor (IGF) I and IGF binding protein (IGFBP) 1 levels in plasma and tissues observed after in vivo administration of lipopolysachcaride (LPS). In overnight-fasted male rats LPS injected via the tail vein decreased the IGF-I concentration in plasma, liver, and skeletal muscle (30-45{\%}) and increased IGF-I content in kidney (~3-fold). LPS also decreased IGF-I mRNA abundance in liver and muscle and increased gene expression in kidney. Concomitantly, IGFBP-1 levels in plasma, liver, and muscle were markedly elevated by LPS. All these changes were associated with a greater than fourfold elevation in plasma corticosterone. Pretreatment of rats with the glucocorticoid receptor antagonist RU-486 completely prevented or blunted the LPS-induced changes in IGF-I content in plasma, liver, muscle, and kidney. In liver and muscle RU-486 significantly attenuated the reduction in IGF-I mRNA abundance produced by LPS, but in kidney the LPS-induced increase in IGF-I mRNA was still evident. In contrast, pretreatment with RU-486 did not prevent or attenuate the LPS-induced increase in IGFBP-1 levels in plasma, liver, or muscle. These data suggest that glucocorticoids play a major role in regulating IGF-I mRNA and peptide content in tissues in response to LPS, but the increased IGFBP-1 in blood and tissues induced by LPS appears largely glucocorticoid independent.",
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Differential role of glucocorticoids in mediating endotoxin-induced changes in IGF-I and IGFBP-1. / Li, Yue Hua; Fan, Jie; Lang, Charles H.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 272, No. 6 41-6, 02.08.1997, p. R1990-R1997.

Research output: Contribution to journalArticle

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AB - The purpose of the present study as to determine whether endogenous elevations in glucocorticoids mediate the changes in insulin-like growth factor (IGF) I and IGF binding protein (IGFBP) 1 levels in plasma and tissues observed after in vivo administration of lipopolysachcaride (LPS). In overnight-fasted male rats LPS injected via the tail vein decreased the IGF-I concentration in plasma, liver, and skeletal muscle (30-45%) and increased IGF-I content in kidney (~3-fold). LPS also decreased IGF-I mRNA abundance in liver and muscle and increased gene expression in kidney. Concomitantly, IGFBP-1 levels in plasma, liver, and muscle were markedly elevated by LPS. All these changes were associated with a greater than fourfold elevation in plasma corticosterone. Pretreatment of rats with the glucocorticoid receptor antagonist RU-486 completely prevented or blunted the LPS-induced changes in IGF-I content in plasma, liver, muscle, and kidney. In liver and muscle RU-486 significantly attenuated the reduction in IGF-I mRNA abundance produced by LPS, but in kidney the LPS-induced increase in IGF-I mRNA was still evident. In contrast, pretreatment with RU-486 did not prevent or attenuate the LPS-induced increase in IGFBP-1 levels in plasma, liver, or muscle. These data suggest that glucocorticoids play a major role in regulating IGF-I mRNA and peptide content in tissues in response to LPS, but the increased IGFBP-1 in blood and tissues induced by LPS appears largely glucocorticoid independent.

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