Lipid-induced lipotoxic damage in liver and hepatocytes of black seabream Acanthopagrus schlegelii is mediated by endoplasmic reticulum stress

Liver is considered the critical tissue for metabolic processing of dietary nutrients including lipids. High-fat diets (HFD) can induce hepatic lipotoxic injury, but the mechanism is unclear. This study aimed to elucidate the underlying role of endoplasmic reticulum stress (ERS) in mediating HFD-ind...

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Autores: Zhao, Wenli, Shen, Yuedong, Bao, Yangguang, Monroig, Óscar, Zhu, Tingting, Sun, Peng, Tocher, Douglas R., Zhou, Qicun, Jin, Min
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2024
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/362152
Acceso en línea:http://hdl.handle.net/10261/362152
Access Level:acceso abierto
Palabra clave:Acanthopagrus schlegelii
High lipid diet
ERS
Lipid accumulation
Cell apoptosis
Lipotoxicity
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oai_identifier_str oai:digital.csic.es:10261/362152
network_acronym_str ES
network_name_str España
repository_id_str
dc.title.none.fl_str_mv Lipid-induced lipotoxic damage in liver and hepatocytes of black seabream Acanthopagrus schlegelii is mediated by endoplasmic reticulum stress
title Lipid-induced lipotoxic damage in liver and hepatocytes of black seabream Acanthopagrus schlegelii is mediated by endoplasmic reticulum stress
spellingShingle Lipid-induced lipotoxic damage in liver and hepatocytes of black seabream Acanthopagrus schlegelii is mediated by endoplasmic reticulum stress
Zhao, Wenli
Acanthopagrus schlegelii
High lipid diet
ERS
Lipid accumulation
Cell apoptosis
Lipotoxicity
title_short Lipid-induced lipotoxic damage in liver and hepatocytes of black seabream Acanthopagrus schlegelii is mediated by endoplasmic reticulum stress
title_full Lipid-induced lipotoxic damage in liver and hepatocytes of black seabream Acanthopagrus schlegelii is mediated by endoplasmic reticulum stress
title_fullStr Lipid-induced lipotoxic damage in liver and hepatocytes of black seabream Acanthopagrus schlegelii is mediated by endoplasmic reticulum stress
title_full_unstemmed Lipid-induced lipotoxic damage in liver and hepatocytes of black seabream Acanthopagrus schlegelii is mediated by endoplasmic reticulum stress
title_sort Lipid-induced lipotoxic damage in liver and hepatocytes of black seabream Acanthopagrus schlegelii is mediated by endoplasmic reticulum stress
dc.creator.none.fl_str_mv Zhao, Wenli
Shen, Yuedong
Bao, Yangguang
Monroig, Óscar
Zhu, Tingting
Sun, Peng
Tocher, Douglas R.
Zhou, Qicun
Jin, Min
author Zhao, Wenli
author_facet Zhao, Wenli
Shen, Yuedong
Bao, Yangguang
Monroig, Óscar
Zhu, Tingting
Sun, Peng
Tocher, Douglas R.
Zhou, Qicun
Jin, Min
author_role author
author2 Shen, Yuedong
Bao, Yangguang
Monroig, Óscar
Zhu, Tingting
Sun, Peng
Tocher, Douglas R.
Zhou, Qicun
Jin, Min
author2_role author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv National Natural Science Foundation of China
National Key Research and Development Program (China)
Guangdong Provincial Key R&D Programme
Zhejiang Province
Ningbo University
Consejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]
dc.subject.none.fl_str_mv Acanthopagrus schlegelii
High lipid diet
ERS
Lipid accumulation
Cell apoptosis
Lipotoxicity
topic Acanthopagrus schlegelii
High lipid diet
ERS
Lipid accumulation
Cell apoptosis
Lipotoxicity
description Liver is considered the critical tissue for metabolic processing of dietary nutrients including lipids. High-fat diets (HFD) can induce hepatic lipotoxic injury, but the mechanism is unclear. This study aimed to elucidate the underlying role of endoplasmic reticulum stress (ERS) in mediating HFD-induced hepatic lipotoxic injury in black seabream (Acanthopagrus schlegelii) via in vitro and in vivo experiments. For the in vitro experiment, isolated hepatocytes from black seabream were incubated for 24 h in medium (Control), or medium supplemented with 200 μM oleic acid (OA) alone or in combination with 20 μM 4-phenyl butyric acid (OA + 4-PBA). In the in vivo experiment, black seabream juveniles (3.30 ± 0.10 g) were fed diets containing lipid at 12.4% (Control) or 18.6% (HFD) for 8 weeks, after which the HFD-fed fish were divided into three groups and, on alternate days over a period of 8 days, subjected to intraperitoneal injections of 50 mg/kg 4-PBA in hydroxypropyl-β-cyclodextrin (HBC) (treatment 4-PBA) or carrier alone (treatment HFD + HBC) versus no injection (HFD). The contents of triglyceride and non-esterified fatty acid, as well as expression levels of genes and proteins involved in lipid metabolism, ERS, apoptosis and inflammation were determined in liver and isolated hepatocytes, and oil-red O staining, ultrastructural observation, flow cytometry assay of apoptosis rate, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining were performed on hepatocytes. The in vitro experiment showed that 4-PBA treatment significantly decreased lipid accumulation, and the OA-induced expression levels of genes/proteins linked to ERS, lipogenesis, inflammation and apoptosis in hepatocytes. Transmission Electron Microscope (TEM) imaging showed that 4-PBA treatment mitigated the ER swelling induced by OA. These results were confirmed in the in vivo experiment, where 4-PBA injection reduced lipid deposition and expression levels of genes/proteins related to ERS, lipogenesis, inflammation and apoptosis in liver compared to the HFD treatment. In conclusion, these results confirmed that ERS plays a contributing regulatory role in HFD- and OA-induced lipotoxic damage including lipid accumulation, apoptosis and inflammation in liver and isolated hepatocytes of black seabream, which supply a new perspective in the cross-talk of ERS and hepatic lipotoxic damage in hepatocytes/liver of marine fish and provide theoretical guidance for the prevention and treatment of hepatic lipotoxic damage.
publishDate 2024
dc.date.none.fl_str_mv 2024
2024
2024
dc.type.none.fl_str_mv info:eu-repo/semantics/article
http://purl.org/coar/resource_type/c_6501
Postprint
info:eu-repo/semantics/acceptedVersion
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10261/362152
url http://hdl.handle.net/10261/362152
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv The underlying dataset has been published as supplementary material of the article in the publisher platform at DOI https://doi.org/10.1016/j.aquaculture.2024.741102
https://doi.org/10.1016/j.aquaculture.2024.741102
Sí
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC
instname:Consejo Superior de Investigaciones Científicas (CSIC)
instname_str Consejo Superior de Investigaciones Científicas (CSIC)
reponame_str DIGITAL.CSIC. Repositorio Institucional del CSIC
collection DIGITAL.CSIC. Repositorio Institucional del CSIC
repository.name.fl_str_mv
repository.mail.fl_str_mv
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spelling Lipid-induced lipotoxic damage in liver and hepatocytes of black seabream Acanthopagrus schlegelii is mediated by endoplasmic reticulum stressZhao, WenliShen, YuedongBao, YangguangMonroig, ÓscarZhu, TingtingSun, PengTocher, Douglas R.Zhou, QicunJin, MinAcanthopagrus schlegeliiHigh lipid dietERSLipid accumulationCell apoptosisLipotoxicityLiver is considered the critical tissue for metabolic processing of dietary nutrients including lipids. High-fat diets (HFD) can induce hepatic lipotoxic injury, but the mechanism is unclear. This study aimed to elucidate the underlying role of endoplasmic reticulum stress (ERS) in mediating HFD-induced hepatic lipotoxic injury in black seabream (Acanthopagrus schlegelii) via in vitro and in vivo experiments. For the in vitro experiment, isolated hepatocytes from black seabream were incubated for 24 h in medium (Control), or medium supplemented with 200 μM oleic acid (OA) alone or in combination with 20 μM 4-phenyl butyric acid (OA + 4-PBA). In the in vivo experiment, black seabream juveniles (3.30 ± 0.10 g) were fed diets containing lipid at 12.4% (Control) or 18.6% (HFD) for 8 weeks, after which the HFD-fed fish were divided into three groups and, on alternate days over a period of 8 days, subjected to intraperitoneal injections of 50 mg/kg 4-PBA in hydroxypropyl-β-cyclodextrin (HBC) (treatment 4-PBA) or carrier alone (treatment HFD + HBC) versus no injection (HFD). The contents of triglyceride and non-esterified fatty acid, as well as expression levels of genes and proteins involved in lipid metabolism, ERS, apoptosis and inflammation were determined in liver and isolated hepatocytes, and oil-red O staining, ultrastructural observation, flow cytometry assay of apoptosis rate, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining were performed on hepatocytes. The in vitro experiment showed that 4-PBA treatment significantly decreased lipid accumulation, and the OA-induced expression levels of genes/proteins linked to ERS, lipogenesis, inflammation and apoptosis in hepatocytes. Transmission Electron Microscope (TEM) imaging showed that 4-PBA treatment mitigated the ER swelling induced by OA. These results were confirmed in the in vivo experiment, where 4-PBA injection reduced lipid deposition and expression levels of genes/proteins related to ERS, lipogenesis, inflammation and apoptosis in liver compared to the HFD treatment. In conclusion, these results confirmed that ERS plays a contributing regulatory role in HFD- and OA-induced lipotoxic damage including lipid accumulation, apoptosis and inflammation in liver and isolated hepatocytes of black seabream, which supply a new perspective in the cross-talk of ERS and hepatic lipotoxic damage in hepatocytes/liver of marine fish and provide theoretical guidance for the prevention and treatment of hepatic lipotoxic damage.This study was supported by the National Natural Science Foundation of China (32273142, 31802303), National Key Research and Development Program of China (2023YFD2400601), “Pioneer” and “Leading Goose” R&D Program of Zhejiang (2024C02006), Guangdong Province Key Research and Development Project (2021B0202050001), Fundamental Research Funds for the Provincial Universities of Zhejiang (SJLY2021007), Open Fund of Zhejiang Provincial Top Key Discipline of Aquaculture in Ningbo University and K. C. Wong Magna Fund in Ningbo University.Peer reviewedElsevierNational Natural Science Foundation of ChinaNational Key Research and Development Program (China)Guangdong Provincial Key R&D ProgrammeZhejiang ProvinceNingbo UniversityConsejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]202420242024info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_6501Postprintinfo:eu-repo/semantics/acceptedVersionapplication/pdfhttp://hdl.handle.net/10261/362152reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)InglésThe underlying dataset has been published as supplementary material of the article in the publisher platform at DOI https://doi.org/10.1016/j.aquaculture.2024.741102https://doi.org/10.1016/j.aquaculture.2024.741102Síinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/3621522026-05-22T06:33:51Z
score 15,812429

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