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

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 i...

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Main Authors: Ritian Jin, Jude Juventus Aweya, Rong Lin, Wuyin Weng, Jiaqi Shang, Dangfeng Wang, Yiling Fan, Shen Yang
Format: Article
Language:English
Published: Elsevier 2023-05-01
Series:Journal of Functional Foods
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S1756464623001159
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author Ritian Jin
Jude Juventus Aweya
Rong Lin
Wuyin Weng
Jiaqi Shang
Dangfeng Wang
Yiling Fan
Shen Yang
author_facet Ritian Jin
Jude Juventus Aweya
Rong Lin
Wuyin Weng
Jiaqi Shang
Dangfeng Wang
Yiling Fan
Shen Yang
author_sort Ritian Jin
collection DOAJ
description 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.
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spelling doaj.art-da66c9431dad4e6dbc80b12288a032172023-04-29T14:48:23ZengElsevierJournal of Functional Foods1756-46462023-05-01104105515The bioactive peptide VLATSGPG regulates the abnormal lipid accumulation and inflammation induced by free fatty acids in HepG2 cells via the PERK signaling pathwayRitian Jin0Jude Juventus Aweya1Rong Lin2Wuyin Weng3Jiaqi Shang4Dangfeng Wang5Yiling Fan6Shen Yang7College of Ocean Food and Biological Engineering, Jimei University, Xiamen 361021, China; Fujian Provincial Key Laboratory of Food Microbiology and Enzyme Engineering, Jimei University, 361021, ChinaCollege of Ocean Food and Biological Engineering, Jimei University, Xiamen 361021, China; Fujian Provincial Key Laboratory of Food Microbiology and Enzyme Engineering, Jimei University, 361021, ChinaCollege of Ocean Food and Biological Engineering, Jimei University, Xiamen 361021, China; Fujian Provincial Key Laboratory of Food Microbiology and Enzyme Engineering, Jimei University, 361021, ChinaCollege of Ocean Food and Biological Engineering, Jimei University, Xiamen 361021, ChinaCollege of Biological and Agricultural Engineering, Jilin University, Changchun 130022, ChinaCollege of Food Science and Technology, Jiangnan University, Wuxi 214122, ChinaCollege of Ocean Food and Biological Engineering, Jimei University, Xiamen 361021, ChinaCollege of Ocean Food and Biological Engineering, Jimei University, Xiamen 361021, China; Fujian Provincial Key Laboratory of Food Microbiology and Enzyme Engineering, Jimei University, 361021, China; Corresponding author at: College of Ocean Food and Biological Engineering, Jimei University, 43 Yindou Road, Xiamen 361021, China.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.http://www.sciencedirect.com/science/article/pii/S1756464623001159DPP-IV inhibitory peptideFree fatty acidsNAFLDPERKHepG2
spellingShingle Ritian Jin
Jude Juventus Aweya
Rong Lin
Wuyin Weng
Jiaqi Shang
Dangfeng Wang
Yiling Fan
Shen Yang
The bioactive peptide VLATSGPG regulates the abnormal lipid accumulation and inflammation induced by free fatty acids in HepG2 cells via the PERK signaling pathway
Journal of Functional Foods
DPP-IV inhibitory peptide
Free fatty acids
NAFLD
PERK
HepG2
title The bioactive peptide VLATSGPG regulates the abnormal lipid accumulation and inflammation induced by free fatty acids in HepG2 cells via the PERK signaling pathway
title_full The bioactive peptide VLATSGPG regulates the abnormal lipid accumulation and inflammation induced by free fatty acids in HepG2 cells via the PERK signaling pathway
title_fullStr The bioactive peptide VLATSGPG regulates the abnormal lipid accumulation and inflammation induced by free fatty acids in HepG2 cells via the PERK signaling pathway
title_full_unstemmed The bioactive peptide VLATSGPG regulates the abnormal lipid accumulation and inflammation induced by free fatty acids in HepG2 cells via the PERK signaling pathway
title_short The bioactive peptide VLATSGPG regulates the abnormal lipid accumulation and inflammation induced by free fatty acids in HepG2 cells via the PERK signaling pathway
title_sort bioactive peptide vlatsgpg regulates the abnormal lipid accumulation and inflammation induced by free fatty acids in hepg2 cells via the perk signaling pathway
topic DPP-IV inhibitory peptide
Free fatty acids
NAFLD
PERK
HepG2
url http://www.sciencedirect.com/science/article/pii/S1756464623001159
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