UM
Skeletal muscle overexpression of short isoform Sirt3 altered mitochondrial cardiolipin content and fatty acid composition
Chabi, Beatrice; Fouret, Gilles; Lecomte, Jerome; Cortade, Fabienne; Pessemesse, Laurence; Baati, Narjes; Coudray, Charles; Lin, Ligen; Tong, Qiang; Wrutniak-Cabello, Chantal; Casas, Francois; Feillet-Coudray, Christine
2018-04
Source PublicationJOURNAL OF BIOENERGETICS AND BIOMEMBRANES
ISSN0145-479X
Volume50Issue:2Pages:131-142
AbstractCardiolipin (CL) is a phospholipid at the heart of mitochondrial metabolism, which plays a key role in mitochondrial function and bioenergetics. Among mitochondrial activity regulators, SIRT3 plays a crucial role in controlling the acetylation status of many enzymes participating in the energy metabolism in particular concerning lipid metabolism and fatty acid oxidation. Data suggest that possible connection may exist between SIRT3 and CL status that has not been evaluated in skeletal muscle. In the present study, we have characterized skeletal muscle lipids as well as mitochondrial lipids composition in mice overexpressing long (SIRT3-M1) and short (SIRT3-M3) isoforms of SIRT3. Particular attention has been paid for CL. We reported no alteration in muscle lipids content and fatty acids composition between the two mice SIRT3 strains and the control mice. However, mitochondrial CL content was significantly decreased in SIRT3-M3 mice and associated to an upregulation of tafazzin gene expression. In addition, mitochondrial phospholipids and fatty acids composition was altered with an increase in the PC/PE ratio and arachidonic acid content and a reduction in the MUFA/SFA ratio. These modifications in mitochondrial membrane composition are associated with a reduction in the enzymatic activities of mitochondrial respiratory chain complexes I and IV. In spite of these mitochondrial enzymatic alterations, skeletal muscle mitochondrial respiration remained similar in SIRT3-M3 and control mice. Surprisingly, none of those metabolic alterations were detected in mitochondria from SIRT3-M1 mice. In conclusion, our data indicate a specific action of the shorter SIRT3 isoform on lipid mitochondrial membrane biosynthesis and functioning.
KeywordSirt3 isoforms Mitochondria Cardiolipin Phospholipids Skeletal muscle
DOI10.1007/s10863-018-9752-1
URLView the original
Indexed BySCI
Language英语
WOS Research AreaBiophysics ; Cell Biology
WOS SubjectBiophysics ; Cell Biology
WOS IDWOS:000429796900005
PublisherSPRINGER/PLENUM PUBLISHERS
The Source to ArticleWOS
Fulltext Access
Citation statistics
Cited Times [WOS]:2   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionUniversity of Macau
Recommended Citation
GB/T 7714
Chabi, Beatrice,Fouret, Gilles,Lecomte, Jerome,et al. Skeletal muscle overexpression of short isoform Sirt3 altered mitochondrial cardiolipin content and fatty acid composition[J]. JOURNAL OF BIOENERGETICS AND BIOMEMBRANES,2018,50(2):131-142.
APA Chabi, Beatrice.,Fouret, Gilles.,Lecomte, Jerome.,Cortade, Fabienne.,Pessemesse, Laurence.,...&Feillet-Coudray, Christine.(2018).Skeletal muscle overexpression of short isoform Sirt3 altered mitochondrial cardiolipin content and fatty acid composition.JOURNAL OF BIOENERGETICS AND BIOMEMBRANES,50(2),131-142.
MLA Chabi, Beatrice,et al."Skeletal muscle overexpression of short isoform Sirt3 altered mitochondrial cardiolipin content and fatty acid composition".JOURNAL OF BIOENERGETICS AND BIOMEMBRANES 50.2(2018):131-142.
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Chabi, Beatrice]'s Articles
[Fouret, Gilles]'s Articles
[Lecomte, Jerome]'s Articles
Baidu academic
Similar articles in Baidu academic
[Chabi, Beatrice]'s Articles
[Fouret, Gilles]'s Articles
[Lecomte, Jerome]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Chabi, Beatrice]'s Articles
[Fouret, Gilles]'s Articles
[Lecomte, Jerome]'s Articles
Terms of Use
No data!
Social Bookmark/Share
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.