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Mitochondrial DNA and Epigenetics: Investigating Interactions with the One‐Carbon Metabolism in Obesity

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cris.virtual.author-orcid0000-0002-7402-1328
cris.virtual.author-orcid0000-0003-4570-7221
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cris.virtual.author-orcid0000-0002-2045-0709
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cris.virtualsource.author-orcid14660f62-2ba1-4e26-9583-d521a27f42e9
cris.virtualsource.author-orcid59851afa-3d5d-435f-95ee-4130cbd454a0
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cris.virtualsource.author-orcid20ac3fe1-f398-4ef7-ab0b-a6a20460f69f
dc.abstract.enMitochondrial DNA copy number (mtDNAcn) has been proposed for use as a surrogate biomarker of mitochondrial health, and evidence suggests that mtDNA might be methylated. Intermediates of the one-carbon cycle (1CC), which is duplicated in the cytoplasm and mitochondria, have a major role in modulating the impact of diet on the epigenome. Moreover, epigenetic pathways and the redox system are linked by the metabolism of glutathione (GSH). In a cohort of 101 normal-weight and 97 overweight/obese subjects, we evaluated mtDNAcn and methylation levels in both mitochondrial and nuclear areas to test the association of these marks with body weight, metabolic profile, and availability of 1CC intermediates associated with diet. Body composition was associated with 1CC intermediate availability. Reduced levels of GSH were measured in the overweight/obese group (p = 1.3∗10−5). A high BMI was associated with lower LINE-1 (p = 0.004) and nominally lower methylenetetrahydrofolate reductase (MTHFR) gene methylation (p = 0.047). mtDNAcn was lower in overweight/obese subjects (p = 0.004) and independently correlated with MTHFR methylation levels (p = 0.005) but not to LINE-1 methylation levels (p = 0.086). DNA methylation has been detected in the light strand but not in the heavy strand of the mtDNA. Although mtDNA methylation in the light strand did not differ between overweight/obese and normal-weight subjects, it was nominally correlated with homocysteine levels (p = 0.035) and MTHFR methylation (p = 0.033). This evidence suggests that increased body weight might perturb mitochondrial-nuclear homeostasis affecting the availability of nutrients acting as intermediates of the one-carbon cycle.
dc.affiliationWydział Nauk o Żywności i Żywieniu
dc.affiliation.instituteKatedra Żywienia Człowieka i Dietetyki
dc.affiliation.instituteKatedra Technologii Żywności Pochodzenia Roślinnego
dc.contributor.authorBordoni, Laura
dc.contributor.authorPetracci, Irene
dc.contributor.authorMłodzik-Czyżewska, Monika
dc.contributor.authorMalinowska, Anna Maria
dc.contributor.authorSzwengiel, Artur
dc.contributor.authorSadowski, Marcin
dc.contributor.authorGabbianelli, Rosita
dc.contributor.authorChmurzyńska, Agata
dc.date.access2026-03-15
dc.date.accessioned2026-03-30T06:38:14Z
dc.date.available2026-03-30T06:38:14Z
dc.date.copyright2022-01-29
dc.date.issued2022
dc.description.abstract<jats:p>Mitochondrial DNA copy number (mtDNAcn) has been proposed for use as a surrogate biomarker of mitochondrial health, and evidence suggests that mtDNA might be methylated. Intermediates of the one‐carbon cycle (1CC), which is duplicated in the cytoplasm and mitochondria, have a major role in modulating the impact of diet on the epigenome. Moreover, epigenetic pathways and the redox system are linked by the metabolism of glutathione (GSH). In a cohort of 101 normal‐weight and 97 overweight/obese subjects, we evaluated mtDNAcn and methylation levels in both mitochondrial and nuclear areas to test the association of these marks with body weight, metabolic profile, and availability of 1CC intermediates associated with diet. Body composition was associated with 1CC intermediate availability. Reduced levels of GSH were measured in the overweight/obese group (<jats:italic>p</jats:italic> = 1.3∗10<jats:sup>−5</jats:sup>). A high BMI was associated with lower LINE‐1 (<jats:italic>p</jats:italic> = 0.004) and nominally lower methylenetetrahydrofolate reductase (<jats:italic>MTHFR</jats:italic>) gene methylation (<jats:italic>p</jats:italic> = 0.047). mtDNAcn was lower in overweight/obese subjects (<jats:italic>p</jats:italic> = 0.004) and independently correlated with <jats:italic>MTHFR</jats:italic> methylation levels (<jats:italic>p</jats:italic> = 0.005) but not to LINE‐1 methylation levels (<jats:italic>p</jats:italic> = 0.086). DNA methylation has been detected in the light strand but not in the heavy strand of the mtDNA. Although mtDNA methylation in the light strand did not differ between overweight/obese and normal‐weight subjects, it was nominally correlated with homocysteine levels (<jats:italic>p</jats:italic> = 0.035) and <jats:italic>MTHFR</jats:italic> methylation (<jats:italic>p</jats:italic> = 0.033). This evidence suggests that increased body weight might perturb mitochondrial‐nuclear homeostasis affecting the availability of nutrients acting as intermediates of the one‐carbon cycle.</jats:p>
dc.description.accesstimeat_publication
dc.description.bibliographyil., bibliogr.
dc.description.financepublication_nocost
dc.description.financecost0,00
dc.description.points100
dc.description.versionfinal_published
dc.description.volume2022
dc.identifier.doi10.1155/2022/9171684
dc.identifier.eissn1942-0994
dc.identifier.issn1942-0900
dc.identifier.urihttps://sciencerep.up.poznan.pl/handle/item/7957
dc.identifier.weblinkhttps://onlinelibrary.wiley.com/doi/10.1155/2022/9171684
dc.languageen
dc.relation.ispartofOxidative Medicine and Cellular Longevity
dc.relation.pagesID 9171684
dc.rightsCC-BY
dc.sciencecloudnosend
dc.share.typeOPEN_JOURNAL
dc.titleMitochondrial DNA and Epigenetics: Investigating Interactions with the One‐Carbon Metabolism in Obesity
dc.typeJournalArticle
dspace.entity.typePublication
oaire.citation.issue1
oaire.citation.volume2022