title: Regenerative capacity differs between micro- and macrovesicular hepatic steatosis.
abstract: BACKGROUND
  Independent of etiology, the hepatic microvesicular steatosis has a worse prognosis compared with macrovesicular steatosis. Proliferation compensates for apoptosis and reflects regenerative mechanisms following liver injury. It is unknown whether these two types of fatty liver have differences in regenerative capacity and apoptosis, which could have an impact on their prognosis.
  
  
  METHODS
  Two groups of pigs were studied for 72 days under a protein-deficient diet. One group received only protein-deficient diet (n=6), the other was treated in addition to the diet with 6g ethanol/kg/day by means of a percutaneous intragastric catheter (n=6). The rate of proliferating and apoptotic hepatocytes was determined, respectively, by proliferation cell nuclear antigen (PCNA) and ISEL/TUNEL staining for apoptosis in liver biopsies with similar steatosis grade in pigs with micro- or macrovesicular fatty liver.
  
  
  RESULTS
  The ethanol-treated group developed microvesicular steatosis, the other group developed macrovesicular steatosis. Proliferation index was significantly increased in macrovesicular in comparison with microvesicular steatosis (p<0.05). Apoptosis rate was similar in both groups.
  
  
  CONCLUSIONS
  Regeneration, but not apoptosis rate differs between micro- and macrovesicular steatosis. The reduced regenerative capacity in microvesicular steatosis may contribute to the worse prognosis of this subtype of fatty liver disease.
authors.affiliation: Department of Surgery, University of Leipzig, Liebigstr. 20, 04103 Leipzig, Germany.
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Oleszczuk
authors.forename: Michael
authors.initials: M
authors.lastname: Spannbauer
authors.forename: Andrea
authors.initials: A
authors.lastname: Tannapfel
authors.forename: Matthias
authors.initials: M
authors.lastname: Blüher
authors.forename: Jan
authors.initials: J
authors.lastname: Hengstler
authors.forename: Uta-Carolin
authors.initials: UC
authors.lastname: Pietsch
authors.forename: Annette
authors.initials: A
authors.lastname: Schuhmacher
authors.forename: Christian
authors.initials: C
authors.lastname: Wittekind
authors.forename: Johann P
authors.initials: JP
authors.lastname: Hauss
authors.forename: Michael R
authors.initials: MR
authors.lastname: Schön
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002452:Cell Count; D049109:Cell Proliferation / Q000187:drug effects; D002624:Chemistry, Clinical; D022162:Cytoplasmic Vesicles / Q000145:classification / Q000378:metabolism* / Q000473:pathology; D018753:Diet, Protein-Restricted; D004195:Disease Models, Animal; D000431:Ethanol / Q000494:pharmacology; D005235:Fatty Liver, Alcoholic / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D020287:In Situ Nick-End Labeling; D008115:Liver Regeneration / Q000187:drug effects / Q000502:physiology*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011488:Protein Deficiency; D013552:Swine
chemical_list: D018809:Proliferating Cell Nuclear Antigen; D000431:Ethanol