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Am J Physiol Endocrinol Metab 279: E1145-E1158, 2000;
0193-1849/00 $5.00
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Vol. 279, Issue 5, E1145-E1158, November 2000

IGF-I/IGFBP-3 binary complex modulates sepsis-induced inhibition of protein synthesis in skeletal muscle

Elisabeth Svanberg2, Robert A. Frost1, Charles H. Lang1, Jorgen Isgaard3, Leonard S. Jefferson1, Scot R. Kimball1, and Thomas C. Vary1

1 Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, Pennsylvania 17033; and Departments of 2 Surgery and 3 Internal Medicine, Gotenburg University, S-41345 Gotenburg, Sweden

The present study evaluated the ability of insulin-like growth factor I (IGF-I) complexed with IGF binding protein-3 (IGFBP-3) to modulate the sepsis-induced inhibition of protein synthesis in gastrocnemius. Beginning 16 h after the induction of sepsis, either the binary complex or saline was injected twice daily via a tail vein, with measurements made 3 and 5 days later. By day 3, sepsis had reduced plasma IGF-I concentrations ~50% in saline-treated rats. Administration of the binary complex provided exogenous IGF-I to compensate for the sepsis-induced diminished plasma IGF-I. Sepsis decreased rates of protein synthesis in gastrocnemius relative to controls by limiting translational efficiency. Treatment of septic rats with the binary complex for 5 days attenuated the sepsis-induced inhibition of protein synthesis and restored translational efficiency to control values. Assessment of potential mechanisms regulating translational efficiency showed that neither the sepsis-induced change in gastrocnemius content of eukaryotic initiation factor 2B (eIF2B), the amount of eIF4E associated with 4E binding protein-1 (4E-BP1), nor the phosphorylation state of 4E-BP1 or eIF4E were altered by the binary complex. Overall, the results are consistent with the hypothesis that decreases in plasma IGF-I are partially responsible for enhanced muscle catabolism during sepsis.

gastrocnemius; eukaryotic initiation factors; translation initiation


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