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野树莓中矢车菊素-3-O-葡萄糖苷通过诱导自噬和调节肠道微生物群发挥降血糖作用。

Pelargonidin-3--glucoside Derived from Wild Raspberry Exerts Antihyperglycemic Effect by Inducing Autophagy and Modulating Gut Microbiota.

机构信息

Department of Food Science and Nutrition, Zhejiang Key Laboratory for Agro-Food Processing, Zhejiang University, No. 866 Yuhangtang Road, Xihu District, Hangzhou 310058, China.

Ningbo Research Institute, Zhejiang University, Ningbo 315100, China.

出版信息

J Agric Food Chem. 2020 Nov 18;68(46):13025-13037. doi: 10.1021/acs.jafc.9b03338. Epub 2019 Jul 29.

DOI:10.1021/acs.jafc.9b03338
PMID:31322351
Abstract

Increasing evidence indicates that anthocyanins exert beneficial effects on type 2 diabetes (T2D), but the underlying mechanism remains unclear. Herein, the hyperglycemia-lowering effect of Pg3G derived from wild raspberry was investigated on high-glucose/high-fat (HG+HF)-induced hepatocytes and / diabetic mice. Our results indicated that Pg3G promoted glucose uptake in HG+HF-induced hepatocytes. Moreover, Pg3G induced autophagy, whereas autophagy inhibitors blocked the hypoglycemic effect of Pg3G. Transcriptional factor EB (TFEB) was found to be linked to Pg3G-induced autophagy. In vivo study showed that Pg3G treatment contributed to the improvement of glucose tolerance, insulin sensitivity, and induction of autophagy. Furthermore, Pg3G not only modified the gut microbiota composition, as indicated by an increased abundance of , and elevated Bacteroidetes/Firmicutes ratio, but also strengthened the intestinal barrier integrity. This study unveils a novel mechanism that Pg3G attenuates hyperglycemia through inducing autophagy and modulating gut microbiota, which implicates a potential nutritional intervention strategy for T2D.

摘要

越来越多的证据表明,花色苷对 2 型糖尿病(T2D)有有益的影响,但潜在的机制仍不清楚。本文研究了源于野生覆盆子的 Pg3G 对高糖/高脂(HG+HF)诱导的肝细胞和 / 糖尿病小鼠的降血糖作用。我们的结果表明,Pg3G 促进了 HG+HF 诱导的肝细胞中的葡萄糖摄取。此外,Pg3G 诱导自噬,而自噬抑制剂阻断了 Pg3G 的降血糖作用。转录因子 EB(TFEB)被发现与 Pg3G 诱导的自噬有关。体内研究表明,Pg3G 治疗有助于改善葡萄糖耐量、胰岛素敏感性和自噬的诱导。此外,Pg3G 不仅改变了肠道微生物群的组成,如 的丰度增加和厚壁菌门/拟杆菌门比值升高,而且还增强了肠道屏障的完整性。本研究揭示了 Pg3G 通过诱导自噬和调节肠道微生物群来减轻高血糖的新机制,这为 T2D 提供了一种潜在的营养干预策略。

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