title: The anabolic effects of IGF-1 in skeletal muscle after burn injury are not caused by increased cell volume.
abstract: BACKGROUND
  In a recent report, insulin-like growth factor 1 (IGF-1) stimulated protein synthesis and inhibited protein breakdown in skeletal muscle after bum injury. The mechanism of the anabolic effects of IGF-1 in skeletal muscle is not known. We tested the hypotheses that IGF-1 stimulates protein synthesis and inhibits protein breakdown in skeletal muscle secondary to cell swelling and that cell swelling in itself induces an anabolic response in muscle tissue.
  
  
  METHODS
  Extensor digitorum longus muscles from control and burned rats were incubated in the absence or presence of 1 microg/mL of IGF-1. Protein synthesis and breakdown rates were determined by measuring incorporation of 14C-phenylalanine into protein and net release of tyrosine, respectively. Cell volume was measured by determining wet and dry weight and by using 3H-mannitol as an extracellular marker.
  
  
  RESULTS
  IGF-1 stimulated protein synthesis and inhibited protein breakdown in muscles from nonburned and burned rats without influencing cell volume. Incubating muscles in hypo-osmotic medium increased cell volume by 17% and inhibited protein breakdown by 14% but did not influence protein synthesis.
  
  
  CONCLUSIONS
  The anabolic effects of IGF-1 in skeletal muscle are not caused by increased cell volume. The results differ from those reported previously in liver cells in which the anabolic effects of IGF-1 were associated with cell swelling. The role of changes in cell volume in the regulation of protein metabolism may be different in skeletal muscle than in other tissues.
authors.affiliation: Department of Surgery, University of Cincinnati, and Shriners Hospital for Children, OH, USA.
authors.forename: C H
authors.initials: CH
authors.lastname: Fang
authors.forename: B G
authors.initials: BG
authors.lastname: Li
authors.forename: J H
authors.initials: JH
authors.lastname: James
authors.forename: J E
authors.initials: JE
authors.lastname: Fischer
authors.forename: P O
authors.initials: PO
authors.lastname: Hasselgren
mesh_terms: D000818:Animals; D002056:Burns / Q000378:metabolism / Q000473:pathology*; D048429:Cell Size; D003078:Colchicine / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D008297:Male; D008353:Mannitol / Q000378:metabolism; D008870:Microtubules / Q000187:drug effects / Q000502:physiology; D009124:Muscle Proteins / Q000096:biosynthesis; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology*; D010649:Phenylalanine / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014316:Tritium; D014443:Tyrosine / Q000378:metabolism
chemical_list: D009124:Muscle Proteins; D014316:Tritium; D008353:Mannitol; D014443:Tyrosine; D010649:Phenylalanine; D007334:Insulin-Like Growth Factor I; D003078:Colchicine