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Distinctive roles of unsaturated and saturated fatty acids in hyperlipidemic pancreatitis

机译:不饱和和饱和脂肪酸在高脂血症性胰腺炎中的独特作用

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摘要

AIM: To investigate how the saturated and unsaturated fatty acid composition influences the susceptibility of developing acute pancreatitis.METHODS: Primary pancreatic acinar cells were treated with low and high concentrations of different saturated and unsaturated fatty acids, and changes in the cytosolic Ca2+ signal and the expression of protein kinase C (PKC) were measured after treatment.RESULTS: Unsaturated fatty acids at high concentrations, including oleic acid, linoleic acid, palmitoleic acid, docosahexaenoic acid, and arachidonic acid, induced a persistent rise in cytosolic Ca2+ concentrations in acinar cells. Unsaturated fatty acids at low concentrations and saturated fatty acids, including palmitic acid, stearic acid, and triglycerides, at low and high concentrations were unable to induce a rise in Ca2+ concentrations in acinar cells. Unsaturated fatty acids at high concentrations but not saturated fatty acids induced intra-acinar cell trypsin activation and cell damage and increased PKC expression.CONCLUSION: At sufficiently high concentrations, unsaturated fatty acids were able to induce acinar cells injury and promote the development of pancreatitis. Unsaturated fatty acids may play a distinctive role in the pathogenesis of pancreatitis through the activation of PKC family members.
机译:目的:探讨饱和和不饱和脂肪酸的组成如何影响发展中的急性胰腺炎的敏感性。方法:用低浓度和高浓度的不同饱和和不饱和脂肪酸处理原代胰腺腺泡细胞,并改变胞质中的Ca 结果:高浓度的不饱和脂肪酸,包括油酸,亚油酸,棕榈油酸,二十二碳六烯酸和花生四烯酸,可以诱导2+信号和蛋白激酶C(PKC)的表达。腺泡细胞中胞质Ca 2 + 浓度持续升高。低浓度和饱和浓度的低浓度不饱和脂肪酸和棕榈酸,硬脂酸和甘油三酸酯等饱和脂肪酸均无法诱导腺泡细胞中Ca 2 + 浓度的升高。高浓度的不饱和脂肪酸会引起腺泡内胰蛋白酶的活化和细胞损伤,并增加PKC的表达。结论:高浓度的不饱和脂肪酸能够引起腺泡细胞的损伤并促进胰腺炎的发展。不饱和脂肪酸可能通过激活PKC家族成员在胰腺炎的发病机制中发挥独特作用。

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