INSULIN-LIKE GROWTH-FACTOR-I BUT NOT GROWTH-HORMONE ATTENUATES DEXAMETHASONE-INDUCED CATABOLISM IN PARENTERALLY-FED RATS

Background: We demonstrated that recombinant human insulin-like growth factor-I (rhIGF-I) or growth hormone (rhGH) produces identical body w eight gain during total parenteral nutrition (TPN) in surgically-stres sed rats. Our current objective was to evaluate the relative anabolic and metabolic effects associated with administration of rhIGF-I and/or rhGH during hypocaloric TPN in rats with dexamethasone (DEX)-induced catabolism. Methods: Male Sprague-Dawley rats (similar to 270 g) given TPN and DEX were treated with IGF-I and/or GH for 6 days. Two control groups, TPN and DEX, were included. Anabolic response was assessed by change in body protein content and nitrogen balance. Metabolic respon se was assessed by determination of serum concentrations triacylglycer ol, glycerol, and free fatty acids. Results: Compared with GH, IGF-I a ttenuated DEX-induced loss of body protein and decreased serum concent rations of glucose, free fatty acids, glycerol, and triglycerol. Treat ment with IGF-I plus GH showed an anabolic response similar to IGF-I a lone. IGF-I and/or GH increased serum concentrations of IGF-I and IGFB P-3. IGF-I alone increased serum level of IGFBP-5. Conclusion: Adminis tration of IGF-I, but not GH, attenuates DEX-induced protein catabolis m in association with increased insulin sensitivity in rats. Glucocort icoid excess may limit the response to GH therapy during TPN.