title: Disrupted hepatic adiponectin signaling impairs liver regeneration of steatotic rats.
abstract: BACKGROUND
  Individuals with non-alcohol fatty liver disease (NAFLD) exhibit impaired liver regeneration in a clinical setting and animal experiments. Adiponectin signaling is recognized as an important pathway of lipid metabolism, energy expenditure, anti-inflammation, and cellular proliferation. We herein investigate hepatic adiponectin signaling in dietary steatotic murine models undergoing hepatectomy, which has never been explored.
  
  
  METHODS
  Sprague-Dawley rats fed with a normal diet (normal), high fat diet (HF), and a methionine-choline deficiency diet for 1 week (MCD 1W) and 5 weeks (MCD 5W), were used. The animals underwent 70% hepatectomy and were thereafter sacrificed at indicated time points.
  
  
  RESULTS
  MCD 5W and HF displayed decreased Ki-67 labeling index and restituted liver mass compared to normal. Hepatic adiponectin, as well as TNF-α, of MCD5W and HF were increased compared to normal; whereas adiponectin receptor type 1 (AdipoR1) and adiponectin receptor type 2 (AdpoR2) were reciprocally decreased when compared to normal. PPARα, a downstream molecule of AdipoR2 axis, was decreased in MCD 5W compared to normal. Adenosine monophosphate- activated protein kinase (AMPK), a downstream molecule of AdipoR1 axis, was inactivated soon after hepatectomy in normal; whereas activation of AMPK persisted until day 3 after hepatectomy in MCD 5W and HF.
  
  
  CONCLUSIONS
  Reciprocal expression of adiponectin and its receptors in steatotic rats represents a unique form of adiponectin signaling disruption, which might be associated with impaired liver regeneration.
authors: Departments of General Surgery, Chang Gung Memorial Hospital at Linkou, Chang Gung University College of Medicine, Taoyuan, Taiwan.
authors: Chun-Yi
authors: CY
authors: Tsai
authors: Yann-Sheng
authors: YS
authors: Lin
authors: Ta-Sen
authors: TS
authors: Yeh
authors: Chon-Folk
authors: CF
authors: Cheong
authors: Chin-Hui
authors: CH
authors: Chang
authors: Tse-Ching
authors: TC
authors: Chen
authors: Miin-Fu
authors: MF
authors: Chen
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D052242:Adiponectin / Q000235:genetics / Q000502:physiology*; D000818:Animals; D005234:Fatty Liver / Q000503:physiopathology*; D008099:Liver / Q000378:metabolism*; D008115:Liver Regeneration; D008297:Male; D065626:Non-alcoholic Fatty Liver Disease; D047493:PPAR alpha / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D054419:Receptors, Adiponectin / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D052242:Adiponectin; D047493:PPAR alpha; D012333:RNA, Messenger; D054419:Receptors, Adiponectin; D014409:Tumor Necrosis Factor-alpha; D055372:AMP-Activated Protein Kinases