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The Effects and Regulatory Mechanism of Casein-Derived Peptide VLPVPQK in Alleviating Insulin Resistance of HepG2 Cells

文献类型： 外文期刊

作者： Li, Dapeng 1 ; Cao, Jianxin 2 ; Zhang, Jin 2 ; Mu, Tong 2 ; Wang, Rubin 2 ; Li, Huanhuan 2 ; Tang, Honggang 2 ; Chen, Lihong 2 ; Lin, Xiuyu 2 ; Peng, Xinyan 1 ; Zhao, Ke 2 ;

作者机构： 1.Yantai Univ, Coll Life Sci, Yantai 264005, Peoples R China

2.Zhejiang Acad Agr Sci, Hangzhou 310021, Peoples R China

3.Shaanxi Normal Univ, Coll Food Engn & Nutr Sci, Xian 710062, Peoples R China

关键词： VLPVPQK; antioxidant activity; HepG2; glucose uptake; transcriptome

期刊名称：FOODS （ 影响因子：5.2； 五年影响因子：5.5 ）

ISSN：

年卷期： 2023 年 12 卷 13 期

页码：

收录情况： SCI

摘要： The liver plays a key role in keeping the homeostasis of glucose and lipid metabolism. Insulin resistance of the liver induced by extra glucose and lipid ingestion contributes greatly to chronic metabolic disease, which is greatly threatening to human health. The small peptide, VLPVPQK, originating from casein hydrolysates of milk, shows various health-promoting functions. However, the effects of VLPVPQK on metabolic disorders of the liver are still not fully understood. Therefore, in the present study, the effects and regulatory mechanism of VLPVPQK on insulin-resistant HepG2 cells was further investigated. The results showed that VLPVPQK exerted strong scavenging capacities against various free radicals, including oxygen radicals, hydroxyl radicals, and cellular reactive oxygen species. In addition, supplementation of VLPVPQK (62.5, 125, and 250 & mu;M) significantly reversed the high glucose and fat (30 mM glucose and 0.2 mM palmitic acid) induced decrement of glucose uptake in HepG2 cells without affecting cell viability. Furthermore, VLPVPQK intervention affected the transcriptomic profiling of the cells. The differentially expressed (DE) genes (FDR < 0.05, and absolute fold change (FC) > 1.5) between VLPVPQK and the model group were mostly enriched in the carbohydrate metabolism-related KEGG pathways. Interestingly, the expression of two core genes (HKDC1 and G6PC1) involved in the above pathways was dramatically elevated after VLPVPQK intervention, which played a key role in regulating glucose metabolism. Furthermore, supplementation of VLPVPQK reversed the high glucose and fat-induced depression of AKR1B10. Overall, VLPVPQK could alleviate the metabolic disorder of hepatocytes by elevating the glucose uptake and eliminating the ROS, while the HKDC1 and AKR1B10 genes might be the potential target genes and play important roles in the process.

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