PMID- 26519879
OWN - NLM
STAT- MEDLINE
DCOM- 20160311
LR  - 20151124
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 468
IP  - 1-2
DP  - 2015 Dec 4-11
TI  - High fructose consumption induces DNA methylation at PPARalpha and CPT1A promoter 
      regions in the rat liver.
PG  - 185-9
LID - S0006-291X(15)30833-0 [pii]
LID - 10.1016/j.bbrc.2015.10.134 [doi]
AB  - 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 (PPARalpha) 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 PPARalpha and CPT1A. qAMP analysis 
      demonstrated the hypermethylation of promoter regions of PPARalpha 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.
CI  - Copyright (c) 2015 Elsevier Inc. All rights reserved.
FAU - Ohashi, Koji
AU  - Ohashi K
AD  - Department of Clinical Biochemistry, Fujita Health University School of Health 
      Sciences, Toyoake, Japan.
FAU - Munetsuna, Eiji
AU  - Munetsuna E
AD  - Department of Biochemistry, Fujita Health University School of Medicine, Toyoake, 
      Japan.
FAU - Yamada, Hiroya
AU  - Yamada H
AD  - Department of Hygiene, Fujita Health University School of Medicine, Toyoake, 
      Japan. Electronic address: hyamada@fujita-hu.ac.jp.
FAU - Ando, Yoshitaka
AU  - Ando Y
AD  - Department of Joint Research Laboratory of Clinical Medicine, Fujita Health 
      University Hospital, Toyoake, Japan.
FAU - Yamazaki, Mirai
AU  - Yamazaki M
AD  - Department of Clinical Biochemistry, Fujita Health University School of Health 
      Sciences, Toyoake, Japan.
FAU - Taromaru, Nao
AU  - Taromaru N
AD  - Department of Clinical Biochemistry, Fujita Health University School of Health 
      Sciences, Toyoake, Japan.
FAU - Nagura, Ayuri
AU  - Nagura A
AD  - Department of Clinical Biochemistry, Fujita Health University School of Health 
      Sciences, Toyoake, Japan.
FAU - Ishikawa, Hiroaki
AU  - Ishikawa H
AD  - Department of Clinical Biochemistry, Fujita Health University School of Health 
      Sciences, Toyoake, Japan.
FAU - Suzuki, Koji
AU  - Suzuki K
AD  - Department of Public Health, Fujita Health University School of Health Sciences, 
      Toyoake, Japan.
FAU - Teradaira, Ryoji
AU  - Teradaira R
AD  - Department of Clinical Biochemistry, Fujita Health University School of Health 
      Sciences, Toyoake, Japan.
FAU - Hashimoto, Shuji
AU  - Hashimoto S
AD  - Department of Hygiene, Fujita Health University School of Medicine, Toyoake, 
      Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20151028
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (PPAR alpha)
RN  - 0 (RNA, Messenger)
RN  - 30237-26-4 (Fructose)
RN  - EC 2.3.1.21 (Carnitine O-Palmitoyltransferase)
RN  - EC 2.3.1.21 (carnitine palmitoyltransferase-1a, rat)
SB  - IM
MH  - Animals
MH  - Carnitine O-Palmitoyltransferase/*genetics
MH  - *DNA Methylation
MH  - Fructose/*metabolism
MH  - Lipid Metabolism
MH  - Liver/*metabolism
MH  - Male
MH  - PPAR alpha/*genetics
MH  - *Promoter Regions, Genetic
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
OTO - NOTNLM
OT  - Corn syrup
OT  - Dyslipidemia
OT  - Epigenetics
OT  - Gene expression
OT  - Metabolic syndrome
OT  - Nutrition
EDAT- 2015/11/01 06:00
MHDA- 2016/03/12 06:00
CRDT- 2015/11/01 06:00
PHST- 2015/10/21 00:00 [received]
PHST- 2015/10/25 00:00 [accepted]
PHST- 2015/11/01 06:00 [entrez]
PHST- 2015/11/01 06:00 [pubmed]
PHST- 2016/03/12 06:00 [medline]
AID - S0006-291X(15)30833-0 [pii]
AID - 10.1016/j.bbrc.2015.10.134 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2015 Dec 4-11;468(1-2):185-9. doi: 
      10.1016/j.bbrc.2015.10.134. Epub 2015 Oct 28.