title: Increased expression of insulin-like growth factor-I in serum and liver after recombinant human growth hormone administration in thermally injured rats.
abstract: BACKGROUND
  Recombinant human growth hormone (rhGH) has been shown to modulate the hypermetabolic response and the hepatic acute-phase response after thermal injury. In vitro studies, however, demonstrated that rhGH activates insulin-like growth factor-I (IGF-I) gene transcription and production, suggesting that rhGH may exert some of its effects indirectly through IGF-I stimulation. The purpose of this study was to determine the effects of rhGH on serum and hepatic IGF-I in thermally injured rats.
  
  
  METHODS
  Sprague-Dawley rats (56 males) receiving a 60% TBSA third-degree scald burn were randomly divided to receive either rhGH (2.5 mg/kg/day im) or saline (control). Rats were sacrificed on postburn days 1, 2, 5, and 7 and serum IGF-I, hepatic IGF-I mRNA, and IGF-I protein concentration were measured. The physiologic response to changes in IGF-I levels was evaluated by measuring hepatocyte proliferation, total liver protein concentration, and muscle dry/wet weights.
  
  
  RESULTS
  Serum IGF-I was increased from postburn day 1 through day 7 in rats receiving rhGH compared to controls (P < 0.05). Hepatic IGF-I mRNA and IGF-I protein expression were increased from day 1 to 7 after burn in animals receiving rhGH when compared to controls (P < 0.05). Recombinant hGH increased hepatocyte proliferation at 5 days and total liver protein concentration at 5 and 7 days postburn compared to controls (P < 0.05). Muscle dry/wet weights increased in rats receiving rhGH at 7 days after burn compared to controls (P < 0.05).
  
  
  CONCLUSIONS
  Liver and serum IGF-I levels decreased after a thermal injury. Recombinant hGH attenuated this decrease by stimulating hepatic IGF-I expression. Increases in IGF-I were associated with increases in hepatocyte proliferation and protein concentration in liver and muscle.
  
  
  CONCLUSIONS
  We suggest that rhGH modulates the hypermetabolic response through IGF-I stimulation in the hepatic parenchyma.
authors.affiliation: Department of Surgery, University of Texas Medical Branch, Galveston, Texas, 77550, USA.
authors.forename: M G
authors.initials: MG
authors.lastname: Jeschke
authors.forename: M T
authors.initials: MT
authors.lastname: Chrysopoulo
authors.forename: D N
authors.initials: DN
authors.lastname: Herndon
authors.forename: S E
authors.initials: SE
authors.lastname: Wolf
mesh_terms: D000818:Animals; D002056:Burns / Q000097:blood / Q000378:metabolism*; D019382:Human Growth Hormone / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism*; D008099:Liver / Q000166:cytology / Q000378:metabolism*; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values
chemical_list: D012333:RNA, Messenger; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I