title: Colonic GLP-2 is not sufficient to promote jejunal adaptation in a PN-dependent rat model of human short bowel syndrome.
abstract: BACKGROUND
  Bowel resection may lead to short bowel syndrome (SBS), which often requires parenteral nutrition (PN) due to inadequate intestinal adaptation. The objective of this study was to determine the time course of adaptation and proglucagon system responses after bowel resection in a PN-dependent rat model of SBS.
  
  
  METHODS
  Rats underwent jugular catheter placement and a 60% jejunoileal resection + cecectomy with jejunoileal anastomosis or transection control surgery. Rats were maintained exclusively with PN and killed at 4 hours to 12 days. A nonsurgical group served as baseline. Bowel growth and digestive capacity were assessed by mucosal mass, protein, DNA, histology, and sucrase activity. Plasma insulin-like growth factor I (IGF-I) and bioactive glucagon-like peptide 2 (GLP-2) were measured by radioimmunoassay.
  
  
  RESULTS
  Jejunum cellularity changed significantly over time with resection but not transection, peaking at days 3-4 and declining by day 12. Jejunum sucrase-specific activity decreased significantly with time after resection and transection. Colon crypt depth increased over time with resection but not transection, peaking at days 7-12. Plasma bioactive GLP-2 and colon proglucagon levels peaked from days 4-7 after resection and then approached baseline. Plasma IGF-I increased with resection through day 12. Jejunum and colon GLP-2 receptor RNAs peaked by day 1 and then declined below baseline.
  
  
  CONCLUSIONS
  After bowel resection resulting in SBS in the rat, peak proglucagon, plasma GLP-2, and GLP-2 receptor levels are insufficient to promote jejunal adaptation. The colon adapts with resection, expresses proglucagon, and should be preserved when possible in massive intestinal resection.
authors: Department of Nutritional Sciences, University of Wisconsin, Madison, WI 53706, USA.
authors: Matthew C
authors: MC
authors: Koopmann
authors: Xiaowen
authors: X
authors: Liu
authors: Christopher J
authors: CJ
authors: Boehler
authors: Sangita G
authors: SG
authors: Murali
authors: Jens J
authors: JJ
authors: Holst
authors: Denise M
authors: DM
authors: Ney
mesh_terms: D000818:Animals; D003106:Colon / Q000378:metabolism* / Q000601:surgery; D053767:Glucagon-Like Peptide 2 / Q000097:blood / Q000378:metabolism*; D000067758:Glucagon-Like Peptide-2 Receptor; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007583:Jejunum / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D008297:Male; D023421:Models, Animal; D010288:Parenteral Nutrition; D052336:Proglucagon / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018027:Receptors, Glucagon / Q000097:blood; D012778:Short Bowel Syndrome / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D013395:Sucrose / Q000378:metabolism
chemical_list: D053767:Glucagon-Like Peptide 2; D000067758:Glucagon-Like Peptide-2 Receptor; D012333:RNA, Messenger; D018027:Receptors, Glucagon; D052336:Proglucagon; D013395:Sucrose; D007334:Insulin-Like Growth Factor I