Fructose consumption induces hypomethylation of hepatic mitochondrial DNA in rats

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 t...

Full description

Saved in:
Bibliographic Details
Published in:Life sciences (1973) 2016-03, Vol.149, p.146-152
Main Authors: Yamazaki, Mirai, Munetsuna, Eiji, Yamada, Hiroya, Ando, Yoshitaka, Mizuno, Genki, Murase, Yuri, Kondo, Kanako, Ishikawa, Hiroaki, Teradaira, Ryoji, Suzuki, Koji, Ohashi, Koji
Format: Article
Language:English
Subjects:
5-Hydroxymethylcytosine
5-Methylcytosine
Animals
Dietary Sucrose - administration & dosage
Dietary Sucrose - adverse effects
DNA Methylation - drug effects
DNA Methylation - physiology
DNA, Mitochondrial - metabolism
Fructose - administration & dosage
Fructose - adverse effects
Fructose-induced hypomethylation
Liver - drug effects
Liver - metabolism
Male
Metabolic syndrome
Non-alcoholic fatty liver disease
Non-alcoholic Fatty Liver Disease - chemically induced
Non-alcoholic Fatty Liver Disease - metabolism
Rats
Rats, Sprague-Dawley
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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. 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. 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. 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.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2016.02.020