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  • Sehgal, RatikaUniversity of Eastern Finland (författare)

Liver saturated fat content associates with hepatic DNA methylation in obese individuals

  • Artikel/kapitelEngelska2023

Förlag, utgivningsår, omfång ...

  • 2023-02-11
  • Springer Science and Business Media LLC,2023

Nummerbeteckningar

  • LIBRIS-ID:oai:lup.lub.lu.se:b8325efc-dd50-473b-8cb6-6fdbdfe8ae74
  • https://lup.lub.lu.se/record/b8325efc-dd50-473b-8cb6-6fdbdfe8ae74URI
  • https://doi.org/10.1186/s13148-023-01431-xDOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

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Klassifikation

  • Ämneskategori:art swepub-publicationtype
  • Ämneskategori:ref swepub-contenttype

Anmärkningar

  • Background: Accumulation of saturated fatty acids (SFAs) in the liver is known to induce hepatic steatosis and inflammation causing non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). Although SFAs have been shown to affect the epigenome in whole blood, pancreatic islets, and adipose tissue in humans, and genome-wide DNA methylation studies have linked epigenetic changes to NAFLD and NASH, studies focusing on the association of SFAs and DNA methylation in human liver are missing. We, therefore, investigated whether human liver SFA content associates with DNA methylation and tested if SFA-linked alterations in DNA methylation associate with NAFLD-related clinical phenotypes in obese individuals. Results: We identified DNA methylation (Infinium HumanMethylation450 BeadChip) of 3169 CpGs to be associated with liver total SFA content (q-value < 0.05) measured using proton NMR spectroscopy in participants of the Kuopio Obesity Surgery Study (n = 51; mean ± SD:49.3 ± 8.5 years old; BMI:43.7 ± 6.2 kg/m2). Of these 3169 sites, 797 overlapped with previously published NASH-associated CpGs (NASH-SFA), while 2372 CpGs were exclusively associated with SFA (Only-SFA). The corresponding annotated genes of these only-SFA CpGs were found to be enriched in pathways linked to satiety and hunger. Among the 54 genes mapping to these enriched pathways, DNA methylation of CpGs mapping to PRKCA and TSPO correlated with their own mRNA expression (HumanHT-12 Expression BeadChip). In addition, DNA methylation of another ten of these CpGs correlated with the mRNA expression of their neighboring genes (p value < 0.05). The proportion of CpGs demonstrating a correlation of DNA methylation with plasma glucose was higher in NASH-SFA and only-SFA groups, while the proportion of significant correlations with plasma insulin was higher in only-NASH and NASH-SFA groups as compared to all CpGs on the Illumina 450 K array (Illumina, San Diego, CA, USA). Conclusions: Our results suggest that one of the mechanisms how SFA could contribute to metabolic dysregulation in NAFLD is at the level of DNA methylation. We further propose that liver SFA-related DNA methylation profile may contribute more to hyperglycemia, while insulin-related methylation profile is more linked to NAFLD or NASH. Further research is needed to elucidate the molecular mechanisms behind these observations.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Perfilyev, AlexanderLund University,Lunds universitet,Diabetes - epigenetik,Forskargrupper vid Lunds universitet,Diabetes - Epigenetics,Lund University Research Groups,Skåne University Hospital(Swepub:lu)med-apy (författare)
  • Männistö, VilleUniversity of Eastern Finland (författare)
  • Ågren, JyrkiUniversity of Eastern Finland (författare)
  • Nilsson, EmmaLund University,Lunds universitet,Diabetes - epigenetik,Forskargrupper vid Lunds universitet,Diabetes - Epigenetics,Lund University Research Groups,Skåne University Hospital(Swepub:lu)endo-eca (författare)
  • Käkelä, PirjoUniversity of Eastern Finland (författare)
  • Ling, CharlotteLund University,Lunds universitet,Diabetes - epigenetik,Forskargrupper vid Lunds universitet,Diabetes - Epigenetics,Lund University Research Groups,Skåne University Hospital(Swepub:lu)endo-cl0 (författare)
  • de Mello, Vanessa D.University of Eastern Finland (författare)
  • Pihlajamäki, JussiKuopio University Hospital,University of Eastern Finland (författare)
  • University of Eastern FinlandDiabetes - epigenetik (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Clinical Epigenetics: Springer Science and Business Media LLC15:11868-70751868-7083

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