Insulin-like growth factor-I fails to reverse corticosteroid-induced protein catabolism in growing piglets.

Corticosteroids such as dexamethasone (DEX) increase leucine turnover and oxidation in humans and animals, indicating whole body protein catabolism. Recently, interest has been growing in the use of recombinant polypeptides such as GH and IGF-I in reversing various states of catabolism. The aim of our study was to investigate whether IGF-I reverses corticosteroid-induced protein catabolism in rapidly growing piglets. Also, we wanted to determine whether IGF-I attenuates corticosteroid-induced hyperglycemia. To study these questions, we performed leucine kinetic studies and measured blood glucose in eight piglets under postabsorptive conditions. We did three studies in each piglet: baseline, DEX treatment (5 mg/kg/d for 4 d), and DEX plus IGF-I treatment (25 micro g/kg/h for 6 h). DEX increased leucine turnover by 18 +/- 14% (mean +/- SD, p < 0.05), and oxidation by 132 +/- 64% (p < 0.01) over baseline values. Adding IGF-I to DEX treatment failed to reverse these changes in leucine kinetics. Turnover again increased by 18 +/- 8% (p < 0.01), and oxidation by 107 +/- 68% (p < 0.05) over baseline values. Nonoxidative leucine disposal, an indicator for protein synthesis, did not significantly differ after treatment with DEX or with DEX plus IGF-I. Blood glucose values increased over baseline values after DEX treatment, and approached baseline values after DEX plus IGF-I. We conclude that IGF-I attenuates corticosteroid-induced hyperglycemia, but does not reverse corticosteroid-induced protein catabolism in growing piglets.