Literature DB >> 19469536

Acetic acid upregulates the expression of genes for fatty acid oxidation enzymes in liver to suppress body fat accumulation.

Tomoo Kondo1, Mikiya Kishi, Takashi Fushimi, Takayuki Kaga.   

Abstract

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 (PPARalpha) 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. PPARalpha, 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 alpha2 5'-AMP-activated protein kinase (AMPK) by siRNA. In conclusion, AcOH suppresses accumulation of body fat and liver lipids by upregulation of genes for PPARalpha and fatty-acid-oxidation-related proteins by alpha2 AMPK mediation in the liver.

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Year:  2009        PMID: 19469536     DOI: 10.1021/jf900470c

Source DB:  PubMed          Journal:  J Agric Food Chem        ISSN: 0021-8561            Impact factor:   5.279


  57 in total

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Review 10.  Role of gut microbiota and Toll-like receptors in nonalcoholic fatty liver disease.

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