Reduction in endoplasmic reticulum stress activates beige adipocytes differentiation and alleviates high fat diet-induced metabolic phenotypes
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Ji-Min | - |
dc.contributor.author | Park, Soyoung | - |
dc.contributor.author | Lee, Duckgue | - |
dc.contributor.author | Ginting, Rehna Paula | - |
dc.contributor.author | Lee, Man Ryul | - |
dc.contributor.author | Lee, Min-Woo | - |
dc.contributor.author | Han, Jaeseok | - |
dc.date.accessioned | 2021-09-10T05:49:09Z | - |
dc.date.available | 2021-09-10T05:49:09Z | - |
dc.date.issued | 2021-05-01 | - |
dc.identifier.issn | 0925-4439 | - |
dc.identifier.issn | 1879-260X | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/18890 | - |
dc.description.abstract | Endoplasmic reticulum (ER) stress is closely associated with various metabolic diseases, such as obesity and diabetes. Development of beige/brite adipocytes increases thermogenesis and helps to reduce obesity. Although the relationship between ER stress and white adipocytes has been studied considerably, the possible role of ER stress and the unfolded protein response (UPR) induction in beige adipocytes differentiation remain to be investigated. In this study we investigated how ER stress affected beige adipocytes differentiation both in vitro and in vivo. Phosphorylation of eIF2 alpha was transiently decreased in the early phase (day 2), whereas it was induced at the late phase with concomitant induction of C/EBP homologous protein (CHOP) during beige adipocytes differentiation. Forced expression of CHOP inhibited the expression of beige adipocytes markers, including Ucp1, Cox8b, Cidea, Prdm16, and Pgc-1 alpha, following the induction of beige adipocytes differentiation. When ER stress was reduced by the chemical chaperone tauroursodeoxycholic acid (TUDCA), the expression of the beige adipocytes marker uncoupling protein 1 (UCP1) was significantly enhanced in inguinal white adipose tissue (iWAT) and high fat diet (HFD)-induced abnormal metabolic phenotype was improved. In summary, we found that ER stress and the UPR induction were closely involved in beige adipogenesis. These results suggest that modulating ER stress could be a potential therapeutic intervention against metabolic dysfunctions via activation of iWAT browning. | - |
dc.format.extent | 9 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Elsevier BV | - |
dc.title | Reduction in endoplasmic reticulum stress activates beige adipocytes differentiation and alleviates high fat diet-induced metabolic phenotypes | - |
dc.type | Article | - |
dc.publisher.location | 네델란드 | - |
dc.identifier.doi | 10.1016/j.bbadis.2021.166099 | - |
dc.identifier.scopusid | 2-s2.0-85100644092 | - |
dc.identifier.wosid | 000632563900018 | - |
dc.identifier.bibliographicCitation | Biochimica et Biophysica Acta - Molecular Basis of Disease, v.1867, no.5, pp 166099 - 166107 | - |
dc.citation.title | Biochimica et Biophysica Acta - Molecular Basis of Disease | - |
dc.citation.volume | 1867 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 166099 | - |
dc.citation.endPage | 166107 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordAuthor | Adipocyte | - |
dc.subject.keywordAuthor | Browning | - |
dc.subject.keywordAuthor | Endoplasmic reticulum | - |
dc.subject.keywordAuthor | C/EBP homologous protein | - |
dc.subject.keywordAuthor | TUDCA | - |
dc.subject.keywordAuthor | UCP1 | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(31538) 22, Soonchunhyang-ro, Asan-si, Chungcheongnam-do, Republic of Korea+82-41-530-1114
COPYRIGHT 2021 by SOONCHUNHYANG UNIVERSITY ALL RIGHTS RESERVED.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.