Suppr超能文献

不饱和脂肪酸和饱和脂肪酸在高脂血症性胰腺炎中的独特作用。

Distinctive roles of unsaturated and saturated fatty acids in hyperlipidemic pancreatitis.

作者信息

Chang Yu-Ting, Chang Ming-Chu, Tung Chien-Chih, Wei Shu-Chen, Wong Jau-Min

机构信息

Yu-Ting Chang, Ming-Chu Chang, Shu-Chen Wei, Jau-Min Wong, Department of Internal Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei 101, Taiwan.

出版信息

World J Gastroenterol. 2015 Aug 28;21(32):9534-43. doi: 10.3748/wjg.v21.i32.9534.

Abstract

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 Ca(2+) 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 Ca(2+) 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 Ca(2+) 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.

摘要

目的

研究饱和脂肪酸和不饱和脂肪酸组成如何影响急性胰腺炎的易感性。

方法

用低浓度和高浓度的不同饱和脂肪酸和不饱和脂肪酸处理原代胰腺腺泡细胞,处理后检测胞质Ca(2+)信号变化及蛋白激酶C(PKC)的表达。

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,可诱导腺泡细胞胞质Ca(2+)浓度持续升高。低浓度的不饱和脂肪酸以及低浓度和高浓度的饱和脂肪酸,包括棕榈酸、硬脂酸和甘油三酯,均不能诱导腺泡细胞Ca(2+)浓度升高。高浓度的不饱和脂肪酸而非饱和脂肪酸可诱导腺泡细胞内胰蛋白酶激活和细胞损伤,并增加PKC表达。

结论

在足够高的浓度下,不饱和脂肪酸能够诱导腺泡细胞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。

相似文献

引用本文的文献

本文引用的文献

1
Role of pancreatic fat in the outcomes of pancreatitis.胰腺脂肪在胰腺炎预后中的作用。
Pancreatology. 2014 Sep-Oct;14(5):403-8. doi: 10.1016/j.pan.2014.06.004. Epub 2014 Jul 1.
2
Current knowledge of hypertriglyceridemic pancreatitis.高甘油三酯血症性胰腺炎的当前认知
Eur J Intern Med. 2014 Oct;25(8):689-94. doi: 10.1016/j.ejim.2014.08.008. Epub 2014 Sep 27.
3
The role of Ca2+ in the pathophysiology of pancreatitis.钙离子在胰腺炎病理生理学中的作用。
J Physiol. 2014 Jan 15;592(2):269-80. doi: 10.1113/jphysiol.2013.261784. Epub 2013 Jul 29.
6
The acinar cell and early pancreatitis responses.腺泡细胞和早期胰腺炎反应。
Clin Gastroenterol Hepatol. 2009 Nov;7(11 Suppl):S10-4. doi: 10.1016/j.cgh.2009.07.036.
8
Hypertriglyceridemic pancreatitis: presentation and management.高甘油三酯血症性胰腺炎:临床表现与管理
Am J Gastroenterol. 2009 Apr;104(4):984-91. doi: 10.1038/ajg.2009.27. Epub 2009 Mar 17.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验