Fructose consumption induces hypomethylation of hepatic mitochondrial DNA in rats

Mirai Yamazaki, Eiji Munetsuna, Hiroya Yamada, Yoshitaka Ando, Genki Mizuno, Yuri Murase, Kanako Kondo, Hiroaki Ishikawa, Ryoji Teradaira, Koji Suzuki, Koji Ohashi

Research output: Contribution to journalArticlepeer-review

38 Citations (Scopus)


Aims Fructose may play a crucial role in the pathogenesis of metabolic syndrome (MetS). However, the pathogenic mechanism of the fructose-induced MetS has not yet been investigated fully. Recently, several reports have investigated the association between mitochondrial DNA (mtDNA) and MetS. We examined the effect of fructose-rich diets on mtDNA content, transcription, and epigenetic changes. Main methods Four-week-old male Sprague-Dawley rats were offered a 20% fructose solution for 14 weeks. We quantified mRNAs for hepatic mitochondrial genes and analyzed the mtDNA methylation (5-mC and 5-hmC) levels using ELISA kits. Key findings Histological analysis revealed non-alcoholic fatty liver disease (NAFLD) in fructose-fed rats. Hepatic mtDNA content and transcription were higher in fructose-fed rats than in the control group. Global hypomethylation of mtDNA was also observed in fructose-fed rats. Significance We showed that fructose consumption stimulates hepatic mtDNA-encoded gene expression. This phenomenon might be due to epigenetic changes in mtDNA. Fructose-induced mitochondrial epigenetic changes appear to be a novel mechanism underlying the pathology of MetS and NAFLD.

Original languageEnglish
Pages (from-to)146-152
Number of pages7
JournalLife Sciences
Publication statusPublished - 15-03-2016

All Science Journal Classification (ASJC) codes

  • General Pharmacology, Toxicology and Pharmaceutics
  • General Biochemistry,Genetics and Molecular Biology


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