脂肪肝
安普克
葡萄糖稳态
脂质代谢
内科学
内分泌学
脂肪变性
碳水化合物代谢
胰岛素抵抗
蛋白激酶B
胰岛素
胰岛素受体
生物
医学
药理学
化学
生物化学
磷酸化
蛋白激酶A
疾病
作者
Lili Jin,Yuxin Sun,Yuying Li,Hanyu Zhang,Wenxue Yu,Yiling Li,Xin Yi,Saeed A. Alsareii,Qiuyu Wang,Dianbao Zhang
出处
期刊:Peptides
[Elsevier]
日期:2021-06-09
卷期号:143: 170597-170597
被引量:12
标识
DOI:10.1016/j.peptides.2021.170597
摘要
Abstract Metabolic associated fatty liver disease (MAFLD) is the leading common chronic liver disease affecting more than one-quarter of the population worldwide, but no pharmacological therapy was approved specifically. A synthetic peptide AWRK6 developed in our group based on the antimicrobial peptide Dybowskin-2CDYa was found to attenuated diabetes as a novel GLP-1 receptor agonist candidate. The effects of AWRK6 on MAFLD and its underlying mechanisms were investigated in this paper. In high energy diet (HED)-induced MAFLD mice, obesity and hepatic steatosis were alleviated by AWRK6 via intraperitoneal injection. The biochemistry measurements data indicated that the abnormal lipid metabolism was relieved and the glucose metabolism was improved significantly. Further, the phosphorylation of liver PI3K/AKT/AMPK/ACC was elevated significantly by AWRK6 treatment. Moreover, the effects of AWRK6 on lipid accumulation and insulin sensitivity in human cells were verified using oleic acid-induced HepG2 fatty liver cell model and insulin-induced HepG2 cells, respectively. These in vitro and in vivo results demonstrated that the peptide AWRK6 ameliorates MAFLD by improving lipid and glucose metabolism homeostasis, and it is mediated by the PI3K/AKT/AMPK/ACC signaling pathway. Thus, AWRK6 has a potential in preventing MAFLD.
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