title: Effects of a high-fiber diet on hepatocyte apoptosis and liver regeneration after partial hepatectomy in rats with fatty liver.
abstract: BACKGROUND
  The morbidity and mortality that accompany fatty liver may occur as a result of increased apoptosis of hepatocytes and decreased liver regeneration. We determined the effects of a high-fiber diet on hepatocyte apoptosis and liver regeneration after partial hepatectomy in rats with fatty liver.
  
  
  METHODS
  Fatty liver was induced in male Wistar rats weighing around 200 g through feeding of a high-fat diet for 4 weeks. The rats were then randomly assigned to 3 groups that received a high-fat diet, a normal diet, or a high-fiber diet for another 4 weeks. Partial hepatectomy (around 70%) was performed, and rats were killed 6, 24, 48, or 72 hours after hepatectomy. We then measured (1) the ratio of remnant liver weight to body weight and assessed the histology of the remnant liver as indicators of fatty liver, (2) caspase-3 activity and in situ cell death detection of DNA fragmentation as indicators of apoptosis, and (3) 5-bromo-2-deoxyuridine (BrdU) activity and (4) ornithine decarboxylase (ODC) contents in remnant livers as markers of regeneration.
  
  
  RESULTS
  We found that (1) a high-fat diet for 4 weeks can markedly induce fatty liver, (2) apoptosis of hepatocytes is greater in fatty liver than in normal liver (98 +/- 19 vs 36 +/- 7) at 6 hours after partial hepatectomy (p < .05), (3) the capacity of liver regeneration decreases significantly (BrdU index: 30 +/- 5 vs 12 +/- 3, and ODC contents: 604 +/- 48 vs 390 +/- 42 mg/dL) in fatty liver 24 hours after partial hepatectomy (p < .05), (4) a normal diet can partially reverse the effects of fatty liver; (5) a high-fiber diet can significantly reverse the effects of fatty liver (p < .05).
  
  
  CONCLUSIONS
  A high-fiber diet can reverse the negative effects of fatty liver on apoptosis and regenerative capacity after partial hepatectomy.
authors.affiliation: Department of Surgery, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei. hslai@ha.mc.ntu.edu.tw
authors.forename: Hong-Shiee
authors.initials: HS
authors.lastname: Lai
authors.forename: Wen-His
authors.initials: WH
authors.lastname: Lin
authors.forename: Pey-Rong
authors.initials: PR
authors.lastname: Chen
authors.forename: Hsiu-Chuan
authors.initials: HC
authors.lastname: Wu
authors.forename: Po-Huang
authors.initials: PH
authors.lastname: Lee
authors.forename: Wei-Jao
authors.initials: WJ
authors.lastname: Chen
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001835:Body Weight / Q000502:physiology; D001973:Bromodeoxyuridine / Q000378:metabolism; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D053938:DNA Fragmentation; D004043:Dietary Fiber / Q000008:administration & dosage*; D005234:Fatty Liver / Q000178:diet therapy* / Q000601:surgery; D006498:Hepatectomy; D008099:Liver / Q000166:cytology / Q000201:enzymology / Q000254:growth & development*; D008115:Liver Regeneration / Q000187:drug effects*; D008297:Male; D009929:Organ Size; D009955:Ornithine Decarboxylase / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D004043:Dietary Fiber; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases; D009955:Ornithine Decarboxylase; D001973:Bromodeoxyuridine