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Article: Clusterin is involved in mediating the metabolic function of adipose SIRT1

TitleClusterin is involved in mediating the metabolic function of adipose SIRT1
Authors
KeywordsBiological sciences
Cell biology
Molecular physiology
Issue Date21-Jan-2022
PublisherCell Press
Citation
iScience, 2022, v. 25, n. 1 How to Cite?
Abstract

SIRT1 is a metabolic sensor regulating energy homeostasis. The present study revealed that mice with selective overexpression of human SIRT1 in adipose tissue (Adipo-SIRT1) were protected from high-fat diet (HFD)-induced metabolic abnormalities. Adipose SIRT1 was enriched at mitochondria-ER contacts (MERCs) to trigger mitohormesis and unfolded protein response (UPRmt), in turn preventing ER stress. As a downstream target of UPRmt, clusterin was significantly upregulated and acted together with SIRT1 to regulate the protein and lipid compositions at MERCs of adipose tissue. In mice lacking clusterin, HFD-induced metabolic abnormalities were significantly enhanced and could not be prevented by overexpression of SIRT1 in adipose tissue. Treatment with ER stress inhibitors restored adipose SIRT1-mediated beneficial effects on systemic energy metabolism. In summary, adipose SIRT1 facilitated the dynamic interactions and communications between mitochondria and ER, via MERCs, in turn triggering a mild mitochondrial stress to instigate the defense responses against dietary obesity-induced metabolic dysfunctions.


Persistent Identifierhttp://hdl.handle.net/10722/338281
ISSN
2023 Impact Factor: 4.6
2023 SCImago Journal Rankings: 1.497
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhang, P-
dc.contributor.authorKonja, D-
dc.contributor.authorZhang, Y-
dc.contributor.authorXu, A-
dc.contributor.authorLee, IK-
dc.contributor.authorJeon, JH-
dc.contributor.authorBashiri, G-
dc.contributor.authorMitra, A-
dc.contributor.authorWang, Y-
dc.date.accessioned2024-03-11T10:27:41Z-
dc.date.available2024-03-11T10:27:41Z-
dc.date.issued2022-01-21-
dc.identifier.citationiScience, 2022, v. 25, n. 1-
dc.identifier.issn2589-0042-
dc.identifier.urihttp://hdl.handle.net/10722/338281-
dc.description.abstract<p>SIRT1 is a metabolic sensor regulating energy homeostasis. The present study revealed that mice with selective overexpression of human SIRT1 in adipose tissue (Adipo-SIRT1) were protected from high-fat diet (HFD)-induced metabolic abnormalities. Adipose SIRT1 was enriched at mitochondria-ER contacts (MERCs) to trigger mitohormesis and unfolded protein response (UPR<sup>mt</sup>), in turn preventing ER stress. As a downstream target of UPR<sup>mt</sup>, clusterin was significantly upregulated and acted together with SIRT1 to regulate the protein and lipid compositions at MERCs of adipose tissue. In mice lacking clusterin, HFD-induced metabolic abnormalities were significantly enhanced and could not be prevented by overexpression of SIRT1 in adipose tissue. Treatment with ER stress inhibitors restored adipose SIRT1-mediated beneficial effects on systemic energy metabolism. In summary, adipose SIRT1 facilitated the dynamic interactions and communications between mitochondria and ER, via MERCs, in turn triggering a mild mitochondrial stress to instigate the defense responses against dietary obesity-induced metabolic dysfunctions.</p>-
dc.languageeng-
dc.publisherCell Press-
dc.relation.ispartofiScience-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectBiological sciences-
dc.subjectCell biology-
dc.subjectMolecular physiology-
dc.titleClusterin is involved in mediating the metabolic function of adipose SIRT1-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1016/j.isci.2021.103709-
dc.identifier.pmid35072003-
dc.identifier.scopuseid_2-s2.0-85123693434-
dc.identifier.volume25-
dc.identifier.issue1-
dc.identifier.eissn2589-0042-
dc.identifier.isiWOS:000747081300008-
dc.identifier.issnl2589-0042-

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