title: Chronic high-fat diets induce oxide injuries and fibrogenesis of pancreatic cells in rats.
abstract: OBJECTIVE
  The mechanism of pancreatic damages induced by chronic high-fat diets (HFDs) remains unknown. The current study was to detect the involvement of free fatty acids (FFAs) and lipid peroxidation in pancreatic injuries in rats induced by a long-term HFD.
  
  
  METHODS
  Rats of HFD groups (n = 12) were fed with an HFD for 2, 4, 6, 10, and 18 weeks, respectively. Pancreatic malondialdehyde content and the concentration of FFA were measured. Histopathologic changes were observed by Sirius red staining for fibrosis and immunostaining of the pancreatic stellate cells for desmin, alpha-smooth muscle actin, platelet-derived growth factor receptor type beta, and transforming growth factor beta1.
  
  
  RESULTS
  Pancreatic malondialdehyde content, the number of desmin and alpha-SMA positive cells significantly increased in all the HFD groups (P < 0.05). The levels of pancreatic FFA, platelet-derived growth factor receptor type beta, and transforming growth factor beta1 increased in rats of 2-, 4-, and 6-week HFD groups (P < 0.05). These enhancements were accompanied with sequential histopathology alterations that resulted from acute inflammatory response in the early stages of secondary pancreatic fibrosis.
  
  
  CONCLUSIONS
  The results indicate that chronic HFD increased pancreatic FFA and lipid peroxidation associated with pancreatic injuries and collagen synthesis by activated pancreatic stellate cells in rats.
authors.affiliation: Department of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Zhang
authors.forename: Yeqing
authors.initials: Y
authors.lastname: Cui
authors.forename: Li
authors.initials: L
authors.lastname: Fang
authors.forename: Fei
authors.initials: F
authors.lastname: Li
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D002784:Cholesterol / Q000097:blood; D003094:Collagen / Q000378:metabolism; D003893:Desmin / Q000378:metabolism; D004041:Dietary Fats / Q000009:adverse effects / Q000378:metabolism*; D018450:Disease Progression; D005230:Fatty Acids, Nonesterified / Q000378:metabolism*; D005355:Fibrosis; D007150:Immunohistochemistry; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D010179:Pancreas / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D010195:Pancreatitis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020797:Receptor, Platelet-Derived Growth Factor beta / Q000378:metabolism; D012815:Signal Processing, Computer-Assisted; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
chemical_list: D000199:Actins; D002784:Cholesterol; D003094:Collagen; D003893:Desmin; D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; D008315:Malondialdehyde; D020797:Receptor, Platelet-Derived Growth Factor beta; D013482:Superoxide Dismutase; D053773:Transforming Growth Factor beta1; D014280:Triglycerides; C498862:Acta2 protein, rat