title: The nutritional status modulates preservation-reperfusion injury in rat fatty liver.
abstract: BACKGROUND
  Microcirculation disturbances are essential factors of preservation injury in fatty liver. However, hepatocyte injury is also markedly excessive in fatty liver resulting, at least in part, from energy metabolism impairment and oxidative stress. Thus, this study aimed to determine whether nutritional status influences preservation injury in fatty liver and whether energetic substrate supplementation, alone or with a vasodilator, is protective.
  
  
  METHODS
  Normal or fatty livers induced by a choline-deficient diet were isolated from fed and fasted rats, preserved in University of Wisconsin solution at 4 degrees C for 18 h, and then reperfused with Krebs-Henseleit solution at 37 degrees C for 120 min. Fasted rats with fatty liver were also treated as follows: (1) Glucose supplementation: rats had access to a glucose solution for 18 h prior procurement; (2) Prostaglandin (PG): alprostadil was continuously infused during reperfusion; (3) Combined treatment: Glucose supplementation + PG.
  
  
  RESULTS
  Fasting-induced liver injury was significantly greater in fatty than normal liver. In fatty livers from fasted rats, all treatments reduced the alanine aminotransaminase release. Hepatic oxygen consumption improved in the glucose and glucose + PG groups, while PG infusion had no effect. Glucose supplementation did not affect portal pressure, which, in contrast, was reduced in livers receiving PG. Finally, all treatments lowered oxidative injury.
  
  
  CONCLUSIONS
  Preservation injury in fatty liver is greatly related to nutritional status. Energetic substrate supplementation may represent a clinically feasible protective strategy and a multistep approach adding vasodilators could offer further benefit by acting on different pathogenetic mechanisms.
authors.affiliation: Department of Internal Medicine, Cardioangiology, and Hepatology, University of Bologna, Bologna, Italy. paolo.caraceni@unibo.it
authors.forename: Paolo
authors.initials: P
authors.lastname: Caraceni
authors.forename: Marco
authors.initials: M
authors.lastname: Domenicali
authors.forename: Anna
authors.initials: A
authors.lastname: Maria Pertosa
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Maiolini
authors.forename: Ignazio
authors.initials: I
authors.lastname: Grattagliano
authors.forename: Alessandro
authors.initials: A
authors.lastname: Principe
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Palasciano
authors.forename: Franco
authors.initials: F
authors.lastname: Trevisani
authors.forename: Mauro
authors.initials: M
authors.lastname: Bernardi
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D019587:Dietary Supplements; D005215:Fasting; D005234:Fatty Liver / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology; D006003:Glycogen / Q000378:metabolism; D066298:In Vitro Techniques; D008099:Liver / Q000098:blood supply* / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009926:Organ Preservation; D011453:Prostaglandins / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism*
chemical_list: D011453:Prostaglandins; D006003:Glycogen; D000410:Alanine Transaminase; D005947:Glucose