title: Sustained function in atrophying liver tissue after portal branch ligation in the rat.
abstract: BACKGROUND
  Preoperative segmental portal vein occlusion has become a common method to prevent liver failure after extended hepatic resection. To date, it is not elucidated whether atrophy by portal deprivation with concomitant contralateral regeneration leads to impaired liver function. We addressed this question by examining the expression of liver function proteins related to glucose homeostasis and acute-phase response in a corresponding animal model.
  
  
  METHODS
  Male Wistar rats were subjected to either portal branch ligation (PBL), partial hepatectomy (PH), or sham operation (SO). The mRNA expression and chronological distribution of glucose-6-phosphatase (G6P), glucagon receptor (GR), glceraldehyd-3-phosphate-dehydrogenase (GAPDH), albumin, fibronectin, and C1-esterase-inhibitor (C1-Inh) genes were examined by Northern-blot hybridizations. Determinations of serum-glucose and glycogen staining by periodic acid and Schiff were performed to analyze changes in glucose mobilization and storage.
  
  
  RESULTS
  In regenerating liver tissue after PH and PBL, we detected a selective reduction of transcripts encoding G6P during the prereplicative period 6 and 12 h after surgery and a contemporary drop in serum glucose levels. This impairment proved to be more distinct after PH than after PBL. Compared with the residual liver after PH, the level of glycogen disappearance was lower after PBL in the regenerating lobe. In the portal-deprived liver tissue, the expression of genes coding for G6P, GR, GAPDH, albumin, fibronectin, and C1-Inh was not altered compared with the SO group.
  
  
  CONCLUSIONS
  Overall, portal-deprived liver tissue undergoing atrophy retains its liver-specific differentiation and function and helps to maintain homeostasis during the fast regeneration of the non-occluded liver lobe.
authors.affiliation: Department of Hepatobiliary Surgery, University Hospital Hamburg-Eppendorf, Hamburg, Germany.l.mueller@uke.uni-hamburg.de
authors.forename: Lars
authors.initials: L
authors.lastname: Mueller
authors.forename: Rainer
authors.initials: R
authors.lastname: Grotelueschen
authors.forename: Jannine
authors.initials: J
authors.lastname: Meyer
authors.forename: Yogesh K
authors.initials: YK
authors.lastname: Vashist
authors.forename: Awad
authors.initials: A
authors.lastname: Abdulgawad
authors.forename: Christian
authors.initials: C
authors.lastname: Wilms
authors.forename: Christian
authors.initials: C
authors.lastname: Hillert
authors.forename: Xavier
authors.initials: X
authors.lastname: Rogiers
authors.forename: Dieter C
authors.initials: DC
authors.lastname: Broering
mesh_terms: D000209:Acute-Phase Proteins / Q000235:genetics; D000818:Animals; D001284:Atrophy; D001483:Base Sequence; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D017931:DNA Primers; D005353:Fibronectins / Q000235:genetics; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000235:genetics; D006498:Hepatectomy; D008099:Liver / Q000033:anatomy & histology / Q000098:blood supply / Q000473:pathology*; D008297:Male; D023421:Models, Animal; D009929:Organ Size; D016133:Polymerase Chain Reaction; D011169:Portal Vein / Q000601:surgery*; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values; D012709:Serum Albumin / Q000235:genetics; D014158:Transcription, Genetic
chemical_list: D000209:Acute-Phase Proteins; D001786:Blood Glucose; D017931:DNA Primers; D005353:Fibronectins; D012709:Serum Albumin; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases