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Walnut-Derived Peptides Promote Autophagy via the Activation of AMPK/mTOR/ULK1 Pathway to Ameliorate Hyperglycemia in Type 2 Diabetic Mice
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2023-02-19 , DOI: 10.1021/acs.jafc.2c07112
Weiyu Hou 1, 2 , Fanrui Zhao 1, 2 , Li Fang 1, 2 , Xiyan Wang 1, 2 , Dan Wu 1, 2 , Chunlei Liu 1, 2 , Yue Leng 1, 2 , Yawen Gao 1, 2 , Junxi Fu 1, 2 , Ji Wang 1, 2 , Weihong Min 1, 2
Affiliation  

Autophagy flux plays a significant protective role in type 2 diabetes mellitus (T2DM). However, the mechanisms by which autophagy mediates insulin resistance (IR) to ameliorate T2DM remain unclear. This study explored the hypoglycemic effects and mechanisms of walnut-derived peptides (fraction 3–10 kDa and LP5) in streptozotocin and high-fat-diet-induced T2DM mice. Findings revealed that walnut-derived peptides reduced the levels of blood glucose and FINS and ameliorated IR and dyslipidemia. They also increased SOD and GSH-PX activities and inhibited the secretion of TNF-α, IL-6, and IL-1β. Additionally, they increased the levels of ATP, COX, SDH, and MMP of liver mitochondria. Western blotting indicated that walnut-derived peptides up-regulated LC3-II/LC3-I and Beclin-1 expression, while they down-regulated p62 expression, which may be associated with the activation of the AMPK/mTOR/ULK1 pathway. Finally, the AMPK activator (AICAR) and inhibitor (Compound C) were used to verify that LP5 could activate autophagy through the AMPK/mTOR/ULK1 pathway in IR HepG2 cells.

中文翻译:

核桃衍生肽通过激活 AMPK/mTOR/ULK1 通路促进自噬改善 2 型糖尿病小鼠的高血糖

自噬通量在 2 型糖尿病 (T2DM) 中起着重要的保护作用。然而,自噬介导胰岛素抵抗 (IR) 以改善 T2DM 的机制仍不清楚。本研究探讨了核桃衍生肽(3-10 kDa 和 LP5)在链脲佐菌素和高脂肪饮食诱导的 T2DM 小鼠中的降血糖作用和机制。研究结果表明,核桃衍生肽可降低血糖和 FINS 水平,并改善 IR 和血脂异常。他们还增加了 SOD 和 GSH-P X活性并抑制 TNF-α、IL-6 和 IL-1β 的分泌。此外,它们还增加了肝脏线粒体的 ATP、COX、SDH 和 MMP 水平。蛋白质印迹表明,核桃衍生肽上调 LC3-II/LC3-I 和 Beclin-1 表达,同时下调 p62 表达,这可能与 AMPK/mTOR/ULK1 通路的激活有关。最后,使用 AMPK 激活剂 (AICAR) 和抑制剂 (Compound C) 验证 LP5 可以通过 AMPK/mTOR/ULK1 通路在 IR HepG2 细胞中激活自噬。
更新日期:2023-02-19
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