Mechanisms of pancreatic injury induced by long-term high-fat diet intake in rats / 中华肝胆外科杂志

ABSTRACT

Objective To clarify the involvement of the free fatty acids(FFA)and lipid peroxida-tion in rat pancreatic tissue during the development of pancreatic injuries inducecd by long-term high-fat diet.Mehtods The male Sprague-Dawley rats (n=72) were randomized into 6 groups (n=12).One group (group control) received standard chow for 18 weeks, the other five groups (group HFD) were fed with a high-fat diet respectively for 2, 4, 6, 10 and 18 weeks.Serum TG and TCH, the his-topathological changes, pancreatic malondialdehyde (MDA) content, superoxide dismutase (SOD) ac-tivity and the concentration of free fatty acids in pancreatic tissues were examined.Pancreatic fibrosis was assessed using Sirius Red staining.The expression of desmin, a smooth muscle actin (α-SMA), platelet-derived growth factor receptor type β (PDGFRβ) and transforming growth factor131 (TGFβ1) was determined with immunohistochemistry.Results Pancreatic MDA content, the number of desmin and α-SMA positive cells were significantly increased in all the HFD groups.The FFA content, PDGFRβ, and TGFβ1 in pancreatic tissues increased in rats of 2, 4 and 6 week HFD groups accompa-nied with typical histological alternations including edema, capillary vessels hyperplasia, and focal aci-nar degeneration, vaculation of acinar and islet cells.In 6, 10 and 18 weeks HFD groups, the lesions had progressed and acinar cell atrophy, fatty replacement, deposition of hemosiderin, and interstitial collagen deposition were observed.Conclusions The increased amounts of FFA and lipid peroxidant in pancreatic tissues are associated with pancreatic cell injuryies and synthesis of collagen by activated PSCs during the chronic high-fat diet intake.