title: Hepatocyte growth factor supply accelerates compensatory hypertrophy caused by portal branch ligation in normal and jaundiced rats.
abstract: BACKGROUND
  Hepatocyte growth factor (HGF), first identified as the most potent mitogen for hepatocytes, significantly stimulates liver regeneration after hepatectomy. In this report, we examined whether HGF is also useful in accelerating compensatory hypertrophy caused by portal branch ligation in normal and jaundiced rats.
  
  
  METHODS
  Normal and reversible obstructive jaundiced rats underwent portal ligation of the left lateral and median branches, which supply approximately 70% of the total volume of the liver. Simultaneously, the animals were continuously treated with either recombinant human HGF (rhHGF) or vehicle alone via an intraperitoneally implanted osmotic pump. Two and four days after portal ligation, the degree of compensatory hypertrophy in unoccluded lobes was examined by measuring the wet weight ratios of the unoccluded lobes to the whole liver and the 5-bromo-2'-deoxyuridine labeling index of hepatocytes in each group.
  
  
  RESULTS
  The HGF treatment significantly increased the wet weight ratios and the DNA synthesis in nonoccluded lobes 2 and 4 days after portal ligation in both normal and jaundiced rats. Moreover, rhHGF supply promptly decreased serum total bilirubin level in jaundiced rats.
  
  
  CONCLUSIONS
  Continuous rhHGF administration not only accelerates compensatory hypertrophy in normal and jaundiced rats but also ameliorates hyperbilirubinemia in jaundiced rats.
authors.affiliation: Department of Surgery and Surgical Basic Science, Kyoto University School of Medicine, Kyoto, 606-8507, Japan. tokaido@kuhp-kyoto-u.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Kaido
authors.forename: A
authors.initials: A
authors.lastname: Yoshikawa
authors.forename: S
authors.initials: S
authors.lastname: Seto
authors.forename: S
authors.initials: S
authors.lastname: Yamaoka
authors.forename: M
authors.initials: M
authors.lastname: Sato
authors.forename: T
authors.initials: T
authors.lastname: Ishii
authors.forename: K
authors.initials: K
authors.lastname: Inoue
authors.forename: M
authors.initials: M
authors.lastname: Imamura
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D001651:Cholestasis, Extrahepatic / Q000150:complications / Q000209:etiology; D003135:Common Bile Duct / Q000503:physiopathology; D004247:DNA / Q000096:biosynthesis; D017228:Hepatocyte Growth Factor / Q000502:physiology* / Q000627:therapeutic use; D006801:Humans; D006932:Hyperbilirubinemia / Q000188:drug therapy / Q000209:etiology; D006984:Hypertrophy; D007565:Jaundice / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D008026:Ligation; D008099:Liver / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009929:Organ Size; D011169:Portal Vein / Q000503:physiopathology*; D051381:Rats; D011916:Rats, Inbred F344; D011994:Recombinant Proteins; D012016:Reference Values; D013997:Time Factors
chemical_list: D011994:Recombinant Proteins; D017228:Hepatocyte Growth Factor; D004247:DNA