Fasting induces hepatic lipid accumulation by stimulating peroxisomal dicarboxylic acid oxidation
Xiao Zhang, Ting Gao, Senwen Deng, Lin Shang, Xiaocui Chen, Kai Chen, Ping Li, Xiaojuan Cui, Jia Zeng
Abstract
ratio and led to an accumulation of 3-OH-CoA and 2-enoyl-CoA intermediates in the liver. This further induced feedback suppression of mitochondrial β-oxidation and promoted hepatic lipid deposition and steatosis. Specific inhibition of peroxisomal β-oxidation attenuated fasting-induced lipid deposition in the liver by reducing succinate production and enhancing mitochondrial fatty acid oxidation. We conclude that suppression of mitochondrial β-oxidation by oxidation of dicarboxylic acids serves as a mechanism for fasting-induced hepatic lipid accumulation and identifies cross talk between peroxisomal and mitochondrial fatty acid oxidation.
Topics & Concepts
PeroxisomeBeta oxidationKetone bodiesInternal medicineFatty acidLipid oxidationEndocrinologyChemistryBiochemistryDicarboxylic acidMitochondrionLipid metabolismBiologyMetabolismReceptorMedicineAntioxidantPeroxisome Proliferator-Activated ReceptorsDiet and metabolism studiesLiver Disease Diagnosis and Treatment