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Dietary p ‐coumaric acid modulates hepatic gene expression involved with lipid metabolism in rats (829.6)
Author(s) -
Kishida Kunihiro,
Suzuki Masaya,
Ihara Hayato
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.829.6
Subject(s) - fatty acid synthase , carbohydrate responsive element binding protein , sterol regulatory element binding protein , lipid metabolism , cholesterol 7 alpha hydroxylase , lipogenesis , endocrinology , medicine , cholesterol , sterol , ldl receptor , chemistry , biochemistry , transcription factor , gene expression , metabolism , biology , lipoprotein , gene
p ‐Coumaric acid (pCA) is a phenolic acid that is ubiquitous in edible plant. pCA has been reported to reduce plasma and hepatic lipids in rats. However the detailed mechanism remains to be elucidated. The aim of this study was to investigate how pCA affected hepatic gene expression involved with lipid metabolism in rats. Male SD rats were fed a western diet (high‐fat, high‐cholesterol, and high‐sucrose) containing 0.2% pCA for 35 days. Dietary pCA attenuated hepatic triacylglycerol and cholesterol accumulation although serum lipid profile was not changed. The hepatic expression of lipogenic genes, acetyl‐CoA carboxylase 1 (ACC1), fatty acid synthase (FAS), malic enzyme (ME), stearoyl‐CoA desaturase 1 (SCD1) was significantly up‐regulated, while their transcription factors, sterol regulatory element binding protein 1c (SREBP1c) and carbohydrate‐responsive element binding protein (ChREBP) were not changed. As for cholesterol metabolism, cholesterol 7α‐hydroxylase (CYP7A1) was down‐regulated, and low density lipoprotein receptor (LDLr) and its transcription factor, sterol regulatory element binding protein 2 (SREBP2) were up‐regulated significantly. These results suggest that pCA improved hepatic lipid accumulation and the variations in mRNA expression might occur as a result of decreased triacylglycerol and cholesterol levels in liver.