title: Effect of high-fat enteral nutrition on hepatocyte injury in response to hemorrhagic shock in the rat.
abstract: BACKGROUND
  High-fat enteral nutrition reduces the inflammatory response following hemorrhagic shock in the rat.
  
  
  OBJECTIVE
  We hypothesized that this intervention might also ameliorate the remote organ injury to the liver associated with this model.
  
  
  METHODS
  Male Sprague-Dawley rats were either starved or fed low-fat or high-fat isocaloric isonitrogenous feed prior to nonlethal hemorrhagic shock induced by a 40% reduction in the blood volume. Animals were sacrificed at 90 minutes or 24 hours after injury. Liver cell damage was assessed by histology and long polymerase chain reaction (PCR) to detect mitochondrial DNA damage. Stress protein expression was measured by Western blot and mRNA expression by real-time PCR and immunohistochemistry.
  
  
  RESULTS
  Animals fed a low-fat diet had the same severity of liver injury as starved animals and increased expression of stress proteins. Animals fed a high-fat diet had minimal liver injury, no evidence of mitochondrial DNA damage, and significantly lower expression of stress proteins. This effect is associated with preservation of hepatocellular morphology, attenuation of mitochondrial DNA damage, and a reduced stress protein response to injury.
  
  
  CONCLUSIONS
  High-fat enteral nutrition protects the liver from the remote effects of hemorrhagic shock, but the mechanism of this effect is not yet known.
authors.affiliation: Tissue Injury and Repair Group, MRC Centre for Inflammation Research Medical School, University of Edinburgh, Teviot Place, Edinburgh, EH8 9AG, UK.
authors.forename: Mary M
authors.initials: MM
authors.lastname: Chu
authors.forename: Misha D P
authors.initials: MD
authors.lastname: Luyer
authors.forename: Nicholas M
authors.initials: NM
authors.lastname: Wheelhouse
authors.forename: Christopher O
authors.initials: CO
authors.lastname: Bellamy
authors.forename: Jan Willem M
authors.initials: JW
authors.lastname: Greve
authors.forename: Wim A
authors.initials: WA
authors.lastname: Buurman
authors.forename: Kathryn
authors.initials: K
authors.lastname: Sangster
authors.forename: Kenneth C H
authors.initials: KC
authors.lastname: Fearon
authors.forename: James A
authors.initials: JA
authors.lastname: Ross
authors.forename: O James
authors.initials: OJ
authors.lastname: Garden
authors.forename: Cornelis H C
authors.initials: CH
authors.lastname: Dejong
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Wigmore
mesh_terms: D000818:Animals; D015153:Blotting, Western; D004249:DNA Damage; D004041:Dietary Fats / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D004750:Enteral Nutrition; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000032:analysis / Q000378:metabolism; D007150:Immunohistochemistry; D008099:Liver / Q000378:metabolism; D008107:Liver Diseases / Q000209:etiology / Q000517:prevention & control*; D008297:Male; D008930:Mitochondria, Liver / Q000235:genetics; D018832:Molecular Chaperones / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000150:complications*
chemical_list: D004041:Dietary Fats; D018840:HSP70 Heat-Shock Proteins; D018832:Molecular Chaperones; D051547:Heme Oxygenase-1