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Updated: Mar 25, 2026
Methodology for Accurate Detection of Mitochondrial DNA Methylation
Published on: May 20, 2018
Fructose consumption induces hypomethylation of hepatic mitochondrial DNA in rats
Mirai Yamazaki1, Eiji Munetsuna2, Hiroya Yamada3
1Department of Clinical Biochemistry, Fujita Health University School of Health Sciences, Toyoake, Japan.
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 14weeks. 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.
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