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 weight gain during total parenteral nutrition (TPN) in surgically-stressed 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 (approximately 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 response was assessed by determination of serum concentrations of IGF-I, IGF binding proteins (IGFBPs), insulin, glucose, triacylglycerol, glycerol, and free fatty acids. RESULTS: Compared with GH, IGF-I attenuated DEX-induced loss of body protein and decreased serum concentrations of glucose, free fatty acids, glycerol, and triglycerol. Treatment with IGF-I plus GH showed an anabolic response similar to IGF-I alone. IGF-I and/or GH increased serum concentrations of IGF-I and IGFBP-3. IGF-I alone increased serum level of IGFBP-5. CONCLUSION: Administration of IGF-I, but not GH, attenuates DEX-induced protein catabolism in association with increased insulin sensitivity in rats. Glucocorticoid excess may limit the response to GH therapy during TPN.