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山药多糖对 TNF-α诱导的 FL83B 细胞胰岛素抵抗的抑制作用。

Inhibitory effects of dioscorea polysaccharide on TNF-α-induced insulin resistance in mouse FL83B cells.

机构信息

Department of Biochemical Science and Technology, College of Life Science, National Taiwan University, Taipei, Taiwan.

出版信息

J Agric Food Chem. 2011 May 25;59(10):5279-85. doi: 10.1021/jf200651c. Epub 2011 Apr 20.

DOI:10.1021/jf200651c
PMID:21476604
Abstract

Dioscorea is a traditional medicinal food in Asia. This study investigated the anti-insulin resistance of dioscorea polysaccharide (DPS) in inflammatory factor (tumor necrosis factor-α; TNF-α) induced mouse normal liver FL83B cells. Insulin resistance was induced by treating cells with TNF-α (20 ng/mL) for 5 h; subsequently, the medium was replaced with insulin and DPS for 60 min of incubation (model 1; alleviating group). In addition, cells were cotreated with TNF-α and DPS for 5 h in model 2 (preventing group). DPS effectively increased glucose uptake and glucose transporter 2 (GLUT2) expression of insulin-resistant cells. Furthermore, DPS stimulated insulin receptor substrate (IRS) tyrosyl phosphorylation and increased p-Akt level to alleviate insulin resistance in models 1 and 2. Finally, the possible mechanism of DPS promoting insulin sensitivity in TNF-α-induced FL83B cells was investigated in this study. DPS may attenuate c-Jun N-terminal kinases (JNK) and insulin resistance caused by TNF-α induction; therefore, DPS also elevated the levels of p-IRS(Tyr) and p-Akt(Ser) to improve insulin sensitivity in the TNF-α-induced FL83B cells.

摘要

山药是亚洲传统的药食同源食品。本研究探讨了山药多糖(DPS)在炎症因子(肿瘤坏死因子-α;TNF-α)诱导的正常鼠肝 FL83B 细胞胰岛素抵抗中的作用。用 TNF-α(20ng/ml)处理细胞 5 小时诱导胰岛素抵抗;然后,用胰岛素和 DPS 孵育 60 分钟更换培养基(模型 1;缓解组)。此外,在模型 2 中(预防组),细胞与 TNF-α和 DPS 共同孵育 5 小时。DPS 有效增加了胰岛素抵抗细胞的葡萄糖摄取和葡萄糖转运蛋白 2(GLUT2)的表达。此外,DPS 刺激胰岛素受体底物(IRS)酪氨酸磷酸化,并增加 p-Akt 水平,从而缓解模型 1 和 2 中的胰岛素抵抗。最后,本研究探讨了 DPS 在 TNF-α诱导的 FL83B 细胞中促进胰岛素敏感性的可能机制。DPS 可能减轻 c-Jun N-末端激酶(JNK)和 TNF-α诱导的胰岛素抵抗;因此,DPS 还提高了 p-IRS(Tyr)和 p-Akt(Ser)的水平,以改善 TNF-α诱导的 FL83B 细胞的胰岛素敏感性。

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