失调
胰岛素抵抗
肠道菌群
毛螺菌科
拟杆菌
脂肪肝
内分泌学
脂肪变性
内科学
血脂异常
胰岛素
非酒精性脂肪肝
生物
厚壁菌
医学
免疫学
生物化学
糖尿病
细菌
16S核糖体RNA
疾病
基因
遗传学
作者
Haoran Chen,Yun Sun,Haiding Zhao,Xiaofen Qi,Hui Cui,Qiming Li,Ying Ma
出处
期刊:Food & Function
[The Royal Society of Chemistry]
日期:2022-01-01
卷期号:13 (19): 9878-9892
被引量:13
摘要
The progression of nonalcoholic fatty liver disease (NAFLD) is closely related to insulin resistance and gut microbiota. Dietary interventions have emerged as effective palliative strategies for NAFLD. The present study investigated the potential mechanisms by which α-lactalbumin peptide Asp-Gln-Trp (DQW) ameliorated insulin resistance and gut microbiota dysbiosis in high-fat diet (HFD)-induced NAFLD mice. The results demonstrated that DQW treatment alleviated HFD-induced body weight gain, hepatic steatosis, insulin resistance, and dyslipidemia. DQW treatment also increased the ratio of Bacteroides to Firmicutes in the gut, reduced the relative abundance of pathogenic bacteria (such as Bacteroides, Blautia, and Alistipes) and enhanced the relative abundance of short-chain fatty acid (SCFA)-producing bacteria (such as Muribaculaceae, Lachnospiraceae_NK4A136_group, and Rikenellaceae_RC9_gut_group). DQW treatment promoted the production of SCFAs and subsequently improved intestinal barrier integrity and inflammation. Furthermore, the results of real-time quantitative PCR (qRT-PCR) and western blotting further proved that the effects of DQW on the attenuation of hepatic insulin resistance were mediated by the PPARα and IRS1/PI3K/AKT pathways. Taken together, these results indicated that DQW treatment could attenuate HFD-induced NAFLD and insulin resistance by modulating gut microbiota composition, enhancing the SCFA levels, and activating the PPARα and IRS1/PI3K/Akt pathways.
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