Insulin‐Like Growth Factor 1 Stimulates Protein Synthesis and Inhibits Protein Breakdown in Muscle From Burned Rats

Publisher Website
Google Scholar
Abstract
Background: Bum injury is associated with substantial whole‐body protein loss, reflecting mainly a catabolic response in skeletal muscle. Recent studies suggest that treatment with insulin‐like growth factor 1 (IGF‐1) may reverse the catabolic response to burn injury, but the effects of IGF‐1 on muscle protein synthesis and breakdown rates after bum injury are not known. We tested the hypothesis that IGF‐1 blunts the catabolic response in skeletal muscle after burn injury by stimulating protein synthesis and inhibiting protein breakdown and that this effect of IGF‐1 is caused by a direct effect on muscle tissue. Methods: Intact extensor digitorum longus muscles from burned, sham‐burned, and untreated rats were incubated in the absence or presence of different concentrations of IGF‐1. Total and myofibrillar protein breakdown rates were measured as net release of tyrosine and 3‐methylhistidine, respectively. Protein synthesis rates were determined by measuring the incorporation of (U‐14C)‐phenylalanine into protein. Results: IGF‐1 stimulated protein synthesis and inhibited protein breakdown in a dose‐dependent fashion in muscles from burned and unburned rats. The maximal effect of IGF‐1 on protein synthesis was seen at a hormone concentration of 100 ng/mL, whereas protein breakdown was further inhibited when the hormone concentration was increased to 1 μg/mL. Ubiquitin messenger RNA (mRNA) levels were reduced by IGF‐1 in incubated muscles, suggesting that IGF‐1 may inhibit ubiquitin‐dependent protein breakdown. Conclusions: These results suggest that the anabolic effects of IGF‐1 after burn may reflect inhibited protein breakdown and stimulated protein synthesis in skeletal muscle and that this response may be caused by a direct effect of IGF‐1 on muscle tissue. (journal of Parenteral and Enteral Nutrition 21:245–251, 1997)

This publication has 30 references indexed in Scilit: