Acetic Acid Upregulates the Expression of Genes for Fatty Acid Oxidation Enzymes in Liver To Suppress Body Fat Accumulation

被引:291
作者
Kondo, Tomoo [1 ]
Kishi, Mikiya [1 ]
Fushimi, Takashi [1 ]
Kaga, Takayuki [1 ]
机构
[1] Mizkan Grp Corp, Cent Res Inst, Aichi 4758585, Japan
关键词
Acetic acid; acetate; 5 '-AMP-activated protein kinase; peroxisome-proliferator-activated receptor alpha; body weight; body fat; fatty acid oxidation; ACTIVATED PROTEIN-KINASE; RECEPTOR-ALPHA; HEART-DISEASE; RISK-FACTORS; PPAR-ALPHA; GLUCOSE; RATS; ENERGY; VINEGAR; OBESITY;
D O I
10.1021/jf900470c
中图分类号
S [农业科学];
学科分类号
082806 [农业信息与电气工程];
摘要
We investigated the effect of acetic acid (AcOH) on the prevention of obesity in high-fat-fed mice. The mice were intragastrically administrated with water or 0.3 or 1.5% AcOH for 6 weeks. AcOH administration inhibited the accumulation of body fat and hepatic lipids without changing food consumption or skeletal muscle weight. Significant increases were observed in the expressions of genes for peroxisome-proliferator-activated receptor alpha (PPAR alpha) and for fatty-acid-oxidation- and thermogenesis-related proteins: acetyl-CoA oxidase (ACO), carnitine palmitoyl transferase-1 (CPT-1), and uncoupling protein-2 (UCP-2), in the liver of the AcOH-treatment groups. PPAR alpha, ACO, CPT-1, and UCP-2 gene expressions were increased in vitro by acetate addition to HepG2 cells. However, the effects were not observed in cells depleted of alpha 2 5 '-AMP-activated protein kinase (AMPK) by siRNA. In conclusion, AcOH suppresses accumulation of body fat and liver lipids by upregulation of genes for PPAR alpha and fatty-acid-oxidation-related proteins by alpha 2 AMPK mediation in the liver.
引用
收藏
页码:5982 / 5986
页数:5
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