title: Fish omega-3 fatty acids induce liver fibrosis in the treatment of bile duct-ligated rats.
abstract: BACKGROUND
  Biliary atresia-induced cholestasis increases hepatic oxidative stress with eventual progression to cirrhosis and liver failure. Omega-3 fatty acids play a possible role in the regulation of oxidative stress and the improvement of cholestasis.
  
  
  OBJECTIVE
  The goal of the present study is to investigate the role of dietary supplementation of fish omega-3 fatty acids in the reduction of hepatocellular damage by using a rat common bile duct ligation model.
  
  
  METHODS
  Sprague-Dawley rats received either sham or bile duct ligation (BDL) and were divided into four study groups: Sham+saline (Sham+sal) group, Sham+Fish oil (Sham+FO) group, BDL+saline (BDL+sal) group, and BDL+Fish oil (BDL+FO) group. Rats from each group were assigned to receive, besides regular chow, once daily with either normal saline or fish omega-3 fatty acids (0.4 % of its own body weight) via gavage for 10 days. Samples of blood, liver tissue homogenates, and histological studies from different groups were analyzed at the end of the study.
  
  
  RESULTS
  Rats from BDL+FO had significantly impaired liver function as compared to other study groups (p < 0.05 is of significant difference). Ishak scores and the TGF-b1 contents were significantly higher in rats that received BDL+FO, p < 0.05. Contrary to TGF-b1 liver content, rats from the BDL+FO group had the lowest glutathione levels among the study groups, p < 0.05.
  
  
  CONCLUSIONS
  Fish omega-3 fatty acids supplementation, albeit increased tissue content of DHA, tended to increase liver fibrosis in BDL rats, decrease liver glutathione level, and compromise hepatic function; fish oil supplementation to subjects with biliary atresia might be of potential hazard and should be used with caution.
authors.affiliation: Pediatrics Department, Kaohsiung Chang-Gung Memorial Hospital, Chang-Gung University College of Medicine, 123 Ta-Pei Road, Niao Song, Kaohsiung, 833, Taiwan.
authors.forename: Chih-Cheng
authors.initials: CC
authors.lastname: Chen
authors.forename: Chun-Yi
authors.initials: CY
authors.lastname: Ho
authors.forename: Hsio-Chi
authors.initials: HC
authors.lastname: Chaung
authors.forename: You-Lin
authors.initials: YL
authors.lastname: Tain
authors.forename: Chih-Sung
authors.initials: CS
authors.lastname: Hsieh
authors.forename: Fang-Ying
authors.initials: FY
authors.lastname: Kuo
authors.forename: Chun-Yu
authors.initials: CY
authors.lastname: Yang
authors.forename: Li-Tung
authors.initials: LT
authors.lastname: Huang
mesh_terms: D000818:Animals; D001656:Biliary Atresia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D002779:Cholestasis / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D003135:Common Bile Duct / Q000473:pathology; D004195:Disease Models, Animal; D015525:Fatty Acids, Omega-3 / Q000633:toxicity*; D005260:Female; D005978:Glutathione / Q000378:metabolism; D008026:Ligation; D008103:Liver Cirrhosis / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D010743:Phospholipids / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism
chemical_list: D015525:Fatty Acids, Omega-3; D010743:Phospholipids; D053773:Transforming Growth Factor beta1; D014280:Triglycerides; D005978:Glutathione