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

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2002-02, Vol.282 (2), p.528-R536
• Main Authors: Kritsch, K. R, Murali, S, Adamo, M. L, Ney, D. M
• Format: Article
• Language: English
• Subjects: Animal Nutritional Physiological Phenomena; Animals; Antibodies; Dexamethasone - pharmacology; Endocrine System - growth & development; Endocrine System - metabolism; Gene Expression - physiology; Glucocorticoids - pharmacology; Growth Hormone - blood; Insulin-Like Growth Factor Binding Protein 3 - blood; Insulin-Like Growth Factor I - genetics; Insulin-Like Growth Factor I - immunology; Insulin-Like Growth Factor I - metabolism; Liver - cytology; Liver - growth & development; Liver - metabolism; Male; Microsomes - metabolism; Organ Size - drug effects; Parenteral Nutrition, Total; Rats; Rats, Sprague-Dawley; Receptors, Somatotropin - genetics; RNA, Messenger - analysis
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00085.2001

1  Department of Nutritional Sciences, University of Wisconsin, Madison, Wisconsin 53706; and 2  Department of Biochemistry, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78224 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. glucocorticoids; growth hormone; insulin-like growth factor-I, insulin-like growth factor-I binding proteins