The bioactive peptide VLATSGPG regulates the abnormal lipid accumulation and inflammation induced by free fatty acids in HepG2 cells via the PERK signaling pathway. (May 2023)

• Record Type: Journal Article
• Authors: Jin, Ritian; Juventus Aweya, Jude; Lin, Rong; Weng, Wuyin; Shang, Jiaqi; Wang, Dangfeng; Fan, Yiling; Yang, Shen
• Is Part Of: Journal of functional foods. Volume 104(2023)
• Publication Date: 2023-05
• Subjects: DPP-IV inhibitory peptide -- Free fatty acids -- NAFLD -- PERK -- HepG2; VLA VLATSGPG -- PERK protein kinase R-like ER kinase -- FFA free fatty acid -- FAS fatty acid synthase -- eIF2α eukaryotic initiation factor 2α -- NAFLD non-alcohol fatty liver disease -- IκBα inhibitor of NF-κB α -- IR insulin resistance -- CoA coenzyme A -- NF-κB nuclear factor-κB -- NASH non-alcoholic steatohepatitis -- ACC acetyl-CoA carboxylase -- SCD-1 stearyl-CoA dehydrogenase 1 -- JNK c-Jun N-terminal kinase -- AP-1 activator protein-1 -- AKT protein kinase B -- IKK IκB kinase -- IRE1 inositol-requiring enzyme 1 -- ATF activating transcription factor -- Bip immunoglobulin binding protein -- SREBP-1 sterol regulatory element-binding protein 1 -- VLDL very low-density lipoprotein -- DPP-IV dipeptidyl peptidase IV -- ER endoplasmic reticulum -- OA oleic acid -- PA palmitic acid -- MEM minimum essential medium -- ECL electrochemiluminescence -- SDS-PAGE sodium dodecyl sulfate polyacryla mide gel electrophoresis -- PVDF polyvinylidene fluoride -- HRP horseradish peroxidase -- TC total cholesterol -- TG total triglyceride -- HDL high-density lipoprotein -- LDL low-density lipoprotein -- BCA bicinchoninic acid -- TNF-α tumor necrosis factor α -- IL-6 interleukin-6 -- RT-PCR reverse transcription-polymerase chain reaction; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2023.105515
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: VLATSGPG inhibits the activation of PERK. VLATSGPG reduces intracellular lipid accumulation. Cellular inflammation levels are inhibited by VLATSGPG. VLATSGPG inhibits the development of nonalcoholic fatty liver disease. Abstract: VLATSGPG (VLA) was a DPP-IV inhibitory peptide isolated from salmon ( Salmo Salar ) skin. Here, we demonstrated that VLA inhibited the activation of PERK through the AKT signaling pathway. Furthermore, we investigated the effect of VLA on free fatty acid (FFA)-induced lipid accumulation disorder and inflammation in HepG2 cells, elucidating the potential regulatory mechanism in this nonalcoholic fatty liver disease cell model. VLA reduced the mRNA expression of adipogenic factors FAS, ACC, and SCD-1 through the PERK/eIF2α pathway and the level of apolipoprotein B-100 secretion. These may contribute to the reducing FFA-induced lipid accumulation in cells and reducing intracellular lipid levels. In addition, VLA increased IκBα mRNA expression via the PERK/IκBα pathway, inhibited the NF-κB p65 activation, and thus inhibited cell inflammation.