Dexamethasone decreases serum and liver IGF-I and maintains liver IGF-I mRNA in parenterally fed rats

K. R. Kritsch, S. Murali, M. L. Adamo, D. M. Ney

Research output: Contribution to journalArticle

30 Scopus citations

Abstract

Insulin-like growth factor-I (IGF-I) gene expression is regulated by nutritional and hormonal factors. High-dose glucocorticoids decrease food intake, and this confounds studies addressing glucocorticoid effects on IGF-I gene regulation. We investigated alterations in the hepatic IGF-I endocrine system induced by a catabolic dose of dexamethasone (Dex) in rats given adequate nutrition by continuous infusion of total parenteral nutrition (TPN) solution with or without IGF-I administration. The four TPN groups included control, +Dex, +IGF-I, and +IGF-I + Dex (n = 9-11/group). Dex induced a 12% loss of body weight in association with a 50% decrease in hepatic immunoreactive IGF-I, a 10% decrease in serum IGF-I, and no change in steady-state liver IGF-I mRNA or growth hormone (GH) receptor binding. Exogenous IGF-I increased serum IGF-I, attenuated Dex-induced catabolism, and did not reduce hepatic levels of IGF-I and IGF-I mRNA despite decreased serum GH. These data suggest that Dex-induced catabolism is associated with downregulation of the hepatic IGF-I endocrine system at the translational or posttranslational level when adequate nutrition is provided.

Original languageEnglish (US)
Pages (from-to)R528-R536
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume282
Issue number2 51-2
DOIs
StatePublished - 2002

Keywords

  • Glucocorticoids
  • Growth hormone
  • Insulin-like growth factor-I, insulin-like growth factor-I binding proteins

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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