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Elovl2-Ablation Leads to Mitochondrial Membrane Fatty Acid Remodeling and Reduced Efficiency in Mouse Liver Mitochondria
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. Complutense University, Spain.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.ORCID iD: 0000-0002-5769-9022
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
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Number of Authors: 102022 (English)In: Nutrients, E-ISSN 2072-6643, Vol. 14, no 3, article id 559Article in journal (Refereed) Published
Abstract [en]

The fatty acid elongase elongation of very long-chain fatty acids protein 2 (ELOVL2) controls the elongation of polyunsaturated fatty acids (PUFA) producing precursors for omega-3, docosahexaenoic acid (DHA), and omega-6, docosapentaenoic acid (DPAn-6) in vivo. Expectedly, Elovl2-ablation drastically reduced the DHA and DPAn-6 in liver mitochondrial membranes. Unexpectedly, however, total PUFAs levels decreased further than could be explained by Elovl2 ablation. The lipid peroxidation process was not involved in PUFAs reduction since malondialdehyde-lysine (MDAL) and other oxidative stress biomarkers were not enhanced. The content of mitochondrial respiratory chain proteins remained unchanged. Still, membrane remodeling was associated with the high voltage-dependent anion channel (VDAC) and adenine nucleotide translocase 2 (ANT2), a possible reflection of the increased demand on phospholipid transport to the mitochondria. Mitochondrial function was impaired despite preserved content of the respiratory chain proteins and the absence of oxidative damage. Oligomycin-insensitive oxygen consumption increased, and coefficients of respiratory control were reduced by 50%. The mitochondria became very sensitive to fatty acid-induced uncoupling and permeabilization, where ANT2 is involved. Mitochondrial volume and number of peroxisomes increased as revealed by transmission electron microscopy. In conclusion, the results imply that endogenous DHA production is vital for the normal function of mouse liver mitochondria and could be relevant not only for mice but also for human metabolism.

Place, publisher, year, edition, pages
2022. Vol. 14, no 3, article id 559
Keywords [en]
docosahexaenoic acid (DHA) deficiency, mitochondrial function, polyunsaturated fatty acids, membrane permeabilization, oxidative damage markers, adenine nucleotide translocase
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Health Sciences
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URN: urn:nbn:se:su:diva-202398DOI: 10.3390/nu14030559ISI: 000754768000001OAI: oai:DiVA.org:su-202398DiVA, id: diva2:1640365
Available from: 2022-02-24 Created: 2022-02-24 Last updated: 2023-08-28Bibliographically approved

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Talamonti, EmanuelaKalinovich, Anastasia V.Bengtsson, ToreJacobsson, AndersShabalina, Irina G.

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