title: Beneficial effects of growth hormone combined with parenteral nutrition in the management of inflammatory bowel disease: an experimental study.
abstract: BACKGROUND
  Growth hormone (GH) improves net protein anabolism and stimulates wound healing. Although GH is also known to exert the trophic effect on the intestinal tract, its role in the healing of intestinal ulceration is not known. The aim of this study was to evaluate the effects of exogenous GH coinfused with parenteral nutrition (PN) in an experimental model of inflammatory bowel disease in rats.
  
  
  METHODS
  All rats underwent central venous cannulation and were randomized to two groups after induction of small intestinal ulceration with indomethacin. Both groups received the same PN formula. In addition, the GH group (n = 10) received subcutaneous injections of human GH at a dose of 1.0 IU/kg daily for 4 days, whereas the control group (n = 10) received injections of normal saline solution. Nitrogen balance, macroscopic inflammation score, intestinal myeloperoxidase activity, DNA content, and mucosal permeability were determined for each rat. Insulin-like growth factor-I (IGF-I) mRNA was detected by reverse transcription and polymerase chain reaction.
  
  
  RESULTS
  Administration of GH significantly improved the cumulative nitrogen balance, ameliorated the gross inflammation score, and decreased intestinal myeloperoxidase activity. Similarly, intestinal permeability was significantly decreased in the GH group as compared with the control group. GH treatment resulted in increased plasma concentration of IGF-I and IGF-I mRNA expressions in both the liver and the small intestine compared with those in the control group.
  
  
  CONCLUSIONS
  Exogenous GH plays an important role in accelerating intestinal healing in an experimental model of small bowel ulceration in rats. The mechanisms may include the stimulated IGF-I production, which thereafter augments intestinal epithelial cell growth.
authors.affiliation: Department of Pediatric Surgery, Osaka University Medical School, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Chen
authors.forename: R
authors.initials: R
authors.lastname: Nezu
authors.forename: M
authors.initials: M
authors.lastname: Inoue
authors.forename: M
authors.initials: M
authors.lastname: Wasa
authors.forename: Y
authors.initials: Y
authors.lastname: Iiboshi
authors.forename: M
authors.initials: M
authors.lastname: Fukuzawa
authors.forename: S
authors.initials: S
authors.lastname: Kamata
authors.forename: Y
authors.initials: Y
authors.lastname: Takagi
authors.forename: A
authors.initials: A
authors.lastname: Okada
mesh_terms: D000818:Animals; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000235:genetics; D019382:Human Growth Hormone / Q000627:therapeutic use*; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000378:metabolism / Q000628:therapy*; D007334:Insulin-Like Growth Factor I / Q000032:analysis / Q000235:genetics; D007413:Intestinal Mucosa / Q000378:metabolism; D008297:Male; D009584:Nitrogen / Q000378:metabolism; D010288:Parenteral Nutrition; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D012333:RNA, Messenger; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D009584:Nitrogen