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肉豆蔻酸通过持续从头合成神经酰胺,增强棕榈酸诱导的与脂肪营养不良相关的脂毒性和脂肪性肝炎。

Myristic acid potentiates palmitic acid-induced lipotoxicity and steatohepatitis associated with lipodystrophy by sustaning de novo ceramide synthesis.

作者信息

Martínez Laura, Torres Sandra, Baulies Anna, Alarcón-Vila Cristina, Elena Montserrat, Fabriàs Gemma, Casas Josefina, Caballeria Joan, Fernandez-Checa Jose C, García-Ruiz Carmen

机构信息

Cell Death and Proliferation, Institute of Biomedical Research of Barcelona (IIBB), CSIC, Barcelona, Spain.

Liver Unit, Hospital Clinic I Provincial de Barcelona, IDIBAPS and CIBERehd, Barcelona, Spain.

出版信息

Oncotarget. 2015 Dec 8;6(39):41479-96. doi: 10.18632/oncotarget.6286.

Abstract

Palmitic acid (PA) induces hepatocyte apoptosis and fuels de novo ceramide synthesis in the endoplasmic reticulum (ER). Myristic acid (MA), a free fatty acid highly abundant in copra/palmist oils, is a predictor of nonalcoholic steatohepatitis (NASH) and stimulates ceramide synthesis. Here we investigated the synergism between MA and PA in ceramide synthesis, ER stress, lipotoxicity and NASH. Unlike PA, MA is not lipotoxic but potentiated PA-mediated lipoapoptosis, ER stress, caspase-3 activation and cytochrome c release in primary mouse hepatocytes (PMH). Moreover, MA kinetically sustained PA-induced total ceramide content by stimulating dehydroceramide desaturase and switched the ceramide profile from decreased to increased ceramide 14:0/ceramide16:0, without changing medium and long-chain ceramide species. PMH were more sensitive to equimolar ceramide14:0/ceramide16:0 exposure, which mimics the outcome of PA plus MA treatment on ceramide homeostasis, than to either ceramide alone. Treatment with myriocin to inhibit ceramide synthesis and tauroursodeoxycholic acid to prevent ER stress ameliorated PA plus MA induced apoptosis, similar to the protection afforded by the antioxidant BHA, the pan-caspase inhibitor z-VAD-Fmk and JNK inhibition. Moreover, ruthenium red protected PMH against PA and MA-induced cell death. Recapitulating in vitro findings, mice fed a diet enriched in PA plus MA exhibited lipodystrophy, hepatosplenomegaly, increased liver ceramide content and cholesterol levels, ER stress, liver damage, inflammation and fibrosis compared to mice fed diets enriched in PA or MA alone. The deleterious effects of PA plus MA-enriched diet were largely prevented by in vivo myriocin treatment. These findings indicate a causal link between ceramide synthesis and ER stress in lipotoxicity, and imply that the consumption of diets enriched in MA and PA can cause NASH associated with lipodystrophy.

摘要

棕榈酸(PA)可诱导肝细胞凋亡,并在内质网(ER)中促进神经酰胺的从头合成。肉豆蔻酸(MA)是一种在椰干/棕榈油中含量极高的游离脂肪酸,是非酒精性脂肪性肝炎(NASH)的一个预测指标,且能刺激神经酰胺合成。在此,我们研究了MA与PA在神经酰胺合成、内质网应激、脂毒性和NASH方面的协同作用。与PA不同,MA并无脂毒性,但可增强PA介导的原代小鼠肝细胞(PMH)中的脂凋亡、内质网应激、半胱天冬酶-3激活及细胞色素c释放。此外,MA通过刺激脱氢神经酰胺去饱和酶在动力学上维持了PA诱导的总神经酰胺含量,并使神经酰胺谱从神经酰胺14:0/神经酰胺16:0降低转变为升高,而不改变中链和长链神经酰胺种类。与单独使用任何一种神经酰胺相比,PMH对模拟PA加MA处理对神经酰胺稳态影响的等摩尔神经酰胺14:0/神经酰胺16:0暴露更为敏感。用myriocin抑制神经酰胺合成以及用牛磺熊去氧胆酸预防内质网应激可改善PA加MA诱导的凋亡,这与抗氧化剂丁基羟基茴香醚(BHA)、泛半胱天冬酶抑制剂z-VAD-Fmk和JNK抑制所提供的保护作用相似。此外,钌红可保护PMH免受PA和MA诱导的细胞死亡。与单独喂食富含PA或MA饮食的小鼠相比,喂食富含PA加MA饮食的小鼠表现出脂肪营养不良、肝脾肿大、肝脏神经酰胺含量和胆固醇水平升高、内质网应激、肝损伤、炎症和纤维化,这重现了体外研究结果。体内使用myriocin治疗在很大程度上预防了富含PA加MA饮食的有害影响。这些发现表明神经酰胺合成与内质网应激在脂毒性中存在因果联系,并暗示食用富含MA和PA的饮食可导致与脂肪营养不良相关的NASH。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78a5/4747168/c768800ee85c/oncotarget-06-41479-g001.jpg

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