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首页> 外文期刊>Endocrinology >Perilipin is present in islets of Langerhans and protects against lipotoxicity when overexpressed in the beta-cell line INS-1.
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Perilipin is present in islets of Langerhans and protects against lipotoxicity when overexpressed in the beta-cell line INS-1.

机译：Perilipin存在于Langerhans的胰岛中，当在β细胞系INS-1中过表达时，可以防止脂毒性。

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Lipids have been shown to play a dual role in pancreatic beta-cells: a lipid-derived signal appears to be necessary for glucose-stimulated insulin secretion, whereas lipid accumulation causes impaired insulin secretion and apoptosis. The ability of the protein perilipin to regulate lipolysis prompted an investigation of the presence of perilipin in the islets of Langerhans. In this study evidence is presented for perilipin expression in rat, mouse, and human islets of Langerhans as well as the rat clonal beta-cell line INS-1. In rat and mouse islets, perilipin was verified to be present in beta-cells. To examine whether the development of lipotoxicity could be prevented by manipulating the conditions for lipid storage in the beta-cell, INS-1 cells with adenoviral-mediated overexpression of perilipin were exposed to lipotoxic conditions for 72 h. In cells exposed to palmitate, perilipin overexpression caused increased accumulation of triacylglycerols and decreased lipolysis compared with control cells. Whereas glucose-stimulated insulin secretion was retained after palmitate exposure in cells overexpressing perilipin, it was completely abolished in control beta-cells. Thus, overexpression of perilipin appears to confer protection against the development of beta-cell dysfunction after prolonged exposure to palmitate by promoting lipid storage and limiting lipolysis.
机译：脂质已经显示出在胰岛β细胞中的双重作用：脂质衍生的信号似乎是葡萄糖刺激的胰岛素分泌所必需的，而脂质积累则导致胰岛素分泌和细胞凋亡受损。蛋白脂蛋白调节脂解的能力促使人们对朗格​​汉斯胰岛中脂蛋白的存在进行了研究。在这项研究中，提供了在大鼠，小鼠和人类胰岛朗格汉斯以及大鼠克隆β细胞系INS-1中脂蛋白表达的证据。在大鼠和小鼠的胰岛中，证实periplipin存在于β细胞中。为了检查是否可以通过操纵β细胞中脂质存储的条件来预防脂毒性的发展，将腺病毒介导的过脂蛋白的INS-1细胞暴露于脂毒性条件72小时。与对照细胞相比，在暴露于棕榈酸酯的细胞中，周脂素的过度表达导致三酰基甘油的积累增加，脂解作用降低。棕榈酸酯暴露后，在过表达perilipin的细胞中葡萄糖刺激的胰岛素分泌得以保留，而在对照β细胞中则被完全消除。因此，在长期暴露于棕榈酸酯后，过高的脂蛋白似乎可以通过促进脂质存储和限制脂解作用来保护抵抗β细胞功能障碍的发展。

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