Zeng 2017 J Biol Chem

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Zeng J, Deng S, Wang Y, Li P, Tang L, Pang Y (2017) Specific inhibition of acyl-CoA oxidase-1 by an acetylenic acid improves hepatic lipid and reactive oxygen species (ROS) metabolism in rats fed a high fat diet. J Biol Chem 292:3800-9.

» PMID: 28077576

Zeng J, Deng S, Wang Y, Li P, Tang L, Pang Y (2017) J Biol Chem

Abstract: A chronic high fat diet results in hepatic mitochondrial dysfunction and induction of peroxisomal fatty acid oxidation (FAO); whether specific inhibition of peroxisomal FAO benefits mitochondrial FAO and reactive oxygen species (ROS) metabolism remains unclear. In this study a specific inhibitor for the rate-limiting enzyme involved in peroxisomal FAO, acyl-CoA oxidase-1 (ACOX1) was developed and used for the investigation of peroxisomal FAO inhibition upon mitochondrial FAO and ROS metabolism. Specific inhibition of ACOX1 by 10,12-tricosadiynoic acid increased hepatic mitochondrial FAO via activation of the SIRT1-AMPK (adenosine 5'-monophosphate-activated protein kinase) pathway and proliferator activator receptor α and reduced hydrogen peroxide accumulation in high fat diet-fed rats, which significantly decreased hepatic lipid and ROS contents, reduced body weight gain, and decreased serum triglyceride and insulin levels. Inhibition of ACOX1 is a novel and effective approach for the treatment of high fat diet- or obesity-induced metabolic diseases by improving mitochondrial lipid and ROS metabolism.

Bioblast editor: Gnaiger E O2k-Network Lab: CN Shanghai Zenda

Labels: MiParea: Exercise physiology;nutrition;life style 

Stress:Oxidative stress;RONS 

Tissue;cell: Liver  Preparation: Oxidase;biochemical oxidation 

Regulation: Inhibitor