High fructose consumption induces DNA methylation at PPARα and CPT1A promoter regions in the rat liver

Koji Ohashi, Eiji Munetsuna, Hiroya Yamada, Yoshitaka Ando, Mirai Yamazaki, Nao Taromaru, Ayuri Nagura, Hiroaki Ishikawa, Koji Suzuki, Ryoji Teradaira, Shuji Hashimoto

研究成果: Article査読

34 被引用数 (Scopus)

抄録

DNA methylation status is affected by environmental factors, including nutrition. Fructose consumption is considered a risk factor for the conditions that make up metabolic syndrome such as dyslipidemia. However, the pathogenetic mechanism by which fructose consumption leads to metabolic syndrome is unclear. Based on observations that epigenetic modifications are closely related to induction of metabolic syndrome, we hypothesized that fructose-induced metabolic syndrome is caused by epigenetic alterations. Male SD rats were designated to receive water or 20% fructose solution for 14 weeks. mRNA levels for peroxisome proliferator-activated receptor alpha (PPARα) and carnitine palmitoyltransferase 1A (CPT1A) was analyzed using Real-time PCR. Restriction digestion and real-time PCR (qAMP) was used for the analysis of DNA methylation status. Hepatic lipid accumulation was also observed by fructose intake. Fructose feeding also significantly decreased mRNA levels for PPARα and CPT1A. qAMP analysis demonstrated the hypermethylation of promoter regions of PPARα and CTP1A genes. Fructose-mediated attenuated gene expression may be mediated by alterations of DNA methylation status, and pathogenesis of metabolic syndrome induced by fructose relates to DNA methylation status.

本文言語English
ページ(範囲)185-189
ページ数5
ジャーナルBiochemical and Biophysical Research Communications
468
1-2
DOI
出版ステータスPublished - 04-12-2015

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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