安普克
β氧化
过氧化物酶体
肉碱棕榈酰转移酶I
内分泌学
AMP活化蛋白激酶
内科学
脂肪组织
肉碱
化学
下调和上调
产热素
过氧化物酶体增殖物激活受体
产热
生物化学
蛋白激酶A
脂肪酸
受体
酶
生物
基因
医学
作者
Tomoo Kondo,Mikiya Kishi,Takashi Fushimi,Takayuki Kaga
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 α (PPARα) 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. PPARα, 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 α2 5′-AMP-activated protein kinase (AMPK) by siRNA. In conclusion, AcOH suppresses accumulation of body fat and liver lipids by upregulation of genes for PPARα and fatty-acid-oxidation-related proteins by α2 AMPK mediation in the liver.
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