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茯砖茶通过调节肠道微生物群和激活IRS1/PI3K/Akt信号通路来管理高脂饮食/链脲佐菌素诱导的2型糖尿病。

Fu Brick Tea Manages HFD/STZ-Induced Type 2 Diabetes by Regulating the Gut Microbiota and Activating the IRS1/PI3K/Akt Signaling Pathway.

作者信息

Qi Bangran, Ren Daoyuan, Li Ting, Niu Pengfei, Zhang Xiangnan, Yang Xingbin, Xiao Jianbo

机构信息

Shaanxi Engineering Laboratory for Food Green Processing and Safety Control, and Shaanxi Key Laboratory for Hazard Factors Assessment in Processing and Storage of Agricultural Products, College of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi'an 710119, China.

Nutrition and Bromatology Group, Department of Analytical and Food Chemistry, Faculty of Food Science and Technology, University of Vigo, Ourense Campus, E-32004 Ourense, Spain.

出版信息

J Agric Food Chem. 2022 Jul 13;70(27):8274-8287. doi: 10.1021/acs.jafc.2c02400. Epub 2022 Jun 29.

Abstract

The antidiabetic effects of Fu brick tea aqueous extract (FTE) and its underlying molecular mechanism in type 2 diabetes mellitus (T2DM) mice were investigated. FTE treatment significantly relieved dyslipidemia, insulin resistance (IR), and hepatic oxidative stress caused by T2DM. FTE also ameliorated the T2DM-induced gut dysbiosis by decreasing the / (F/B) ratio at the phylum level and promoting the proliferation of , , and at the genus level. Besides, FTE significantly improved colonic short-chain fatty acid levels of T2DM mice. Furthermore, the antidiabetic effects of FTE were proved to be mediated by the IRS1/PI3K/Akt and AMPK-mediated gluconeogenesis signaling pathways. Metabolomics analysis illustrated that FTE recovered the levels of 28 metabolites associated with T2DM to the levels of normal mice. Taken together, these findings suggest that FTE can alleviate T2DM by reshaping the gut microbiota, activating the IRS1/PI3K/Akt pathway, and regulating intestinal metabolites.

摘要

研究了茯砖茶水提取物(FTE)对2型糖尿病(T2DM)小鼠的抗糖尿病作用及其潜在分子机制。FTE治疗显著缓解了T2DM引起的血脂异常、胰岛素抵抗(IR)和肝脏氧化应激。FTE还通过在门水平降低/(F/B)比值和在属水平促进、和的增殖来改善T2DM诱导的肠道菌群失调。此外,FTE显著提高了T2DM小鼠的结肠短链脂肪酸水平。此外,FTE的抗糖尿病作用被证明是由IRS1/PI3K/Akt和AMPK介导的糖异生信号通路介导的。代谢组学分析表明,FTE将28种与T2DM相关的代谢物水平恢复到正常小鼠的水平。综上所述,这些发现表明FTE可以通过重塑肠道微生物群、激活IRS1/PI3K/Akt通路和调节肠道代谢物来缓解T2DM。

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