Mitochondrial peptide Mtln contributes to oxidative metabolism in mice

Mitoregulin (Mtln) is a recently identified 56 amino acid long mitochondrial peptide conserved in vertebrates. Mtln is known to enhance function of respiratory complex I, which is likely mediated by modulation of lipid composition. To address an influence of Mtln gene on the metabolism we created kn...

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Veröffentlicht in:Biochimie 2023-01, Vol.204, p.136-139
Hauptverfasser: Averina, Olga A., Permyakov, Oleg A., Emelianova, Mariia A., Grigoryeva, Olga O., Gulyaev, Mikhail V., Pavlova, Olga S., Mariasina, Sofia S., Frolova, Olga Yu, Kurkina, Marina V., Baydakova, Galina V., Zakharova, Ekaterina Yu, Marey, Maria V., Tsarev, Dmitry A., Tashlitsky, Vadim N., Popov, Vladimir S., Lovat, Maxim L., Polshakov, Vladimir I., Vyssokikh, Mikhail Yu, Sergiev, Petr V.
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container_title Biochimie
container_volume 204
creator Averina, Olga A.
Permyakov, Oleg A.
Emelianova, Mariia A.
Grigoryeva, Olga O.
Gulyaev, Mikhail V.
Pavlova, Olga S.
Mariasina, Sofia S.
Frolova, Olga Yu
Kurkina, Marina V.
Baydakova, Galina V.
Zakharova, Ekaterina Yu
Marey, Maria V.
Tsarev, Dmitry A.
Tashlitsky, Vadim N.
Popov, Vladimir S.
Lovat, Maxim L.
Polshakov, Vladimir I.
Vyssokikh, Mikhail Yu
Sergiev, Petr V.
description Mitoregulin (Mtln) is a recently identified 56 amino acid long mitochondrial peptide conserved in vertebrates. Mtln is known to enhance function of respiratory complex I, which is likely mediated by modulation of lipid composition. To address an influence of Mtln gene on the metabolism we created knockout mice deficient in Mtln gene. In line with accumulation of triglycerides observed earlier on a model of Mtln knockout cell lines, we observed Mtln KO mice to develop obesity on a high fat diet. An increased weight gain could be attributed to enhanced fat accumulation according to the magnetic resonance live imaging. In addition, Mtln KO mice demonstrate elevated serum triglycerides and other oxidation substrates accompanied by an exhaustion of tricarboxylic acids cycle intermediates, suggesting suboptimal oxidation of respiration substrates by mitochondria lacking Mtln.
doi_str_mv 10.1016/j.biochi.2022.09.009
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Mtln is known to enhance function of respiratory complex I, which is likely mediated by modulation of lipid composition. To address an influence of Mtln gene on the metabolism we created knockout mice deficient in Mtln gene. In line with accumulation of triglycerides observed earlier on a model of Mtln knockout cell lines, we observed Mtln KO mice to develop obesity on a high fat diet. An increased weight gain could be attributed to enhanced fat accumulation according to the magnetic resonance live imaging. In addition, Mtln KO mice demonstrate elevated serum triglycerides and other oxidation substrates accompanied by an exhaustion of tricarboxylic acids cycle intermediates, suggesting suboptimal oxidation of respiration substrates by mitochondria lacking Mtln.</abstract><cop>France</cop><pub>Elsevier B.V</pub><pmid>36174793</pmid><doi>10.1016/j.biochi.2022.09.009</doi><tpages>4</tpages></addata></record>
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subjects Animals
Diet, High-Fat - adverse effects
Lipid Metabolism
Metabolism
Mice
Mice, Knockout
Mitochondria
Mitochondria - metabolism
Oxidative phosphorylation
Oxidative Stress
Peptides - metabolism
Short open reading frame
Small peptide
Triglycerides - metabolism
Weight Gain
title Mitochondrial peptide Mtln contributes to oxidative metabolism in mice
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