Cideb facilitates the lipidation of chylomicrons in the small intestine

Cideb facilitates the lipidation of chylomicrons in the small intestine
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Cideb 促进小肠中乳糜微粒的脂化

DOI:
10.1194/jlr.m046482
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发表时间:
2014-07
期刊:
The Journal of Lipid Research
影响因子:
--
通讯作者:
Ye Jing
Ye Jing
中科院分区:
其他
文献类型:
--
作者:
Zhao Yuanlin;Hu Peizhen;Li Peng;Ye Jing

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诱导细胞死亡的dff45样效应物b (Cideb)是一种内质网(ER)和脂滴(LD)相关蛋白,已被证明通过促进VLDL颗粒的脂化和成熟,在维持肝脏脂质稳态中发挥关键作用。本实验中,我们观察到Cideb在小肠空肠和回肠部分表达,其表达是由高脂肪饮食诱导的。脂质灌胃导致cideb缺陷小鼠肠道内脂质滞留。此外,我们观察到,Cideb缺乏小鼠表现出肠道乳糜微粒- tg分泌减少和肠细胞脂质积累增加。cideb缺陷小鼠小肠分泌的乳糜微粒的大小也小于野生型小鼠。此外,Cideb的过表达增加了肠细胞样Caco-2细胞的TG分泌,减少了脂质积累。此外,我们证明了Cideb定位于内质网和ld,并能与Caco-2细胞中的ApoB48相互作用。综上所述,这些数据表明西德布在控制肠道乳糜微粒脂化中起重要作用。
Cell death-inducing DFF45-like effector b (Cideb), an endoplasmic reticulum (ER)- and lipid droplet (LD)-associated protein, has been shown to play a critical role in maintaining hepatic lipid homeostasis by promoting the lipidation and maturation of VLDL particles. Here, we observed that Cideb is expressed in the jejunum and ileum sections of the small intestine, and its expression was induced by high-fat diet. Intragastric gavage with lipids resulted in the retention of lipids in the intestine in Cideb-deficient mice. In addition, we observed that mice with Cideb deficiency exhibited reduced intestinal chylomicron-TG secretion and increased lipid accumulation in the enterocytes. The sizes of chylomicrons secreted from the small intestine of Cideb-deficient mice were also smaller than those from wild-type mice. Furthermore, the overexpression of Cideb increased TG secretion and reduced lipid accumulation in the enterocyte-like Caco-2 cells. In addition, we proved that Cideb was localized to the ER and LDs and could interact with ApoB48 in Caco-2 cells. Overall, these data revealed that Cideb plays an important role in controlling intestinal chylomicron lipidation.
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