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

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)185-189
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume468
Issue number1-2
DOIs
Publication statusPublished - 04-12-2015

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Carnitine O-Palmitoyltransferase
PPAR alpha
DNA Methylation
Fructose
Genetic Promoter Regions
Liver
Rats
Epigenomics
Real-Time Polymerase Chain Reaction
Messenger RNA
Nutrition
Dyslipidemias
Gene expression
Digestion
Genes
Lipids
Gene Expression
Water

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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title = "High fructose consumption induces DNA methylation at PPARα and CPT1A promoter regions in the rat liver",
abstract = "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.",
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High fructose consumption induces DNA methylation at PPARα and CPT1A promoter regions in the rat liver. / Ohashi, Koji; Munetsuna, Eiji; Yamada, Hiroya; Ando, Yoshitaka; Yamazaki, Mirai; Taromaru, Nao; Nagura, Ayuri; Ishikawa, Hiroaki; Suzuki, Koji; Teradaira, Ryoji; Hashimoto, Shuji.

In: Biochemical and Biophysical Research Communications, Vol. 468, No. 1-2, 04.12.2015, p. 185-189.

Research output: Contribution to journalArticle

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T1 - High fructose consumption induces DNA methylation at PPARα and CPT1A promoter regions in the rat liver

AU - Ohashi, Koji

AU - Munetsuna, Eiji

AU - Yamada, Hiroya

AU - Ando, Yoshitaka

AU - Yamazaki, Mirai

AU - Taromaru, Nao

AU - Nagura, Ayuri

AU - Ishikawa, Hiroaki

AU - Suzuki, Koji

AU - Teradaira, Ryoji

AU - Hashimoto, Shuji

PY - 2015/12/4

Y1 - 2015/12/4

N2 - 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.

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