Modulation of inflammation-induced changes in insulin-like growth factor (IGF)-I and IGF binding protein-1 by anti-TNF antibody

Jie Fan, Yue Hua Li, Gregory J. Bagby, Charles H. Lang

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

The aim of the present study was to characterize changes in the insulin-like growth factor (IGF) system produced by the nonbacterial nonendotoxic inflammatory agent zymosan and to determine whether these changes were mediated by enhanced production of tumor necrosis factor (TNF). Rats were injected intraperitoneally with either zymosan or saline and studied 18 h later. Animals were pretreated with either nonimmune IgG or neutralizing anti-TNF antibody 2 h before zymosan injection. Zymosan increased the plasma concentration of TNFα, and this was associated with a decrease (∼40%) in the IGF-I concentration in plasma, liver, heart, and brain. The IGF-I content was not altered in skeletal muscle and kidney. Zymosan also increased the concentration of IGF binding protein (BP)-1 in plasma (120%), liver (90%), and muscle (470%). Circulating TNFα was not detectable in rats injected with anti-TNF antibody before zymosan. The neutralizing antibody prevented the zymosan-induced reduction in IGF-I in plasma and blunted the decreased observed in liver, but did not alter the decrease in heart or brain. Anti-TNF antibody also attenuated (40-60%) the increased IGFBP-1 in plasma, liver, and muscle observed in zymosan-treated rats. We conclude that zymosan-induced inflammation not only decreases IGF-I in plasma and selected tissues, but also increases IGFBP-1 in plasma, liver, and muscle, and that these alterations are due in large part to the enhanced production of TNFα.

Original languageEnglish (US)
Pages (from-to)21-26
Number of pages6
JournalShock
Volume4
Issue number1
DOIs
StatePublished - Jan 1 1995

Fingerprint

Insulin-Like Growth Factor Binding Protein 1
Zymosan
Insulin-Like Growth Factor I
Tumor Necrosis Factor-alpha
Inflammation
Antibodies
Liver
Muscles
Brain
Somatomedins
Neutralizing Antibodies
Skeletal Muscle
Immunoglobulin G
Kidney
Injections

All Science Journal Classification (ASJC) codes

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine

Cite this

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title = "Modulation of inflammation-induced changes in insulin-like growth factor (IGF)-I and IGF binding protein-1 by anti-TNF antibody",
abstract = "The aim of the present study was to characterize changes in the insulin-like growth factor (IGF) system produced by the nonbacterial nonendotoxic inflammatory agent zymosan and to determine whether these changes were mediated by enhanced production of tumor necrosis factor (TNF). Rats were injected intraperitoneally with either zymosan or saline and studied 18 h later. Animals were pretreated with either nonimmune IgG or neutralizing anti-TNF antibody 2 h before zymosan injection. Zymosan increased the plasma concentration of TNFα, and this was associated with a decrease (∼40{\%}) in the IGF-I concentration in plasma, liver, heart, and brain. The IGF-I content was not altered in skeletal muscle and kidney. Zymosan also increased the concentration of IGF binding protein (BP)-1 in plasma (120{\%}), liver (90{\%}), and muscle (470{\%}). Circulating TNFα was not detectable in rats injected with anti-TNF antibody before zymosan. The neutralizing antibody prevented the zymosan-induced reduction in IGF-I in plasma and blunted the decreased observed in liver, but did not alter the decrease in heart or brain. Anti-TNF antibody also attenuated (40-60{\%}) the increased IGFBP-1 in plasma, liver, and muscle observed in zymosan-treated rats. We conclude that zymosan-induced inflammation not only decreases IGF-I in plasma and selected tissues, but also increases IGFBP-1 in plasma, liver, and muscle, and that these alterations are due in large part to the enhanced production of TNFα.",
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Modulation of inflammation-induced changes in insulin-like growth factor (IGF)-I and IGF binding protein-1 by anti-TNF antibody. / Fan, Jie; Li, Yue Hua; Bagby, Gregory J.; Lang, Charles H.

In: Shock, Vol. 4, No. 1, 01.01.1995, p. 21-26.

Research output: Contribution to journalArticle

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