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Down-regulation of tetradecanoylcarnitine by EAS indicated the EAS treatment could recover the dysfunction of VLACD in MPTP-induced PD mice, the therapeutic effects of EAS may base on the regulation of the dysfunction of VLACD in mitochondrial beta-oxidation of long chain saturated fatty acids and fatty acid metabolism.
As a result of this decline in mitochondrial activity less fatty acids can be removed within adipocytes by uncoupled mitochondrial beta-oxidation and by re-esterification, as mitochondrial activity provides substrates for glyceroneogenesis.
Tianeptine, a new tricyclic antidepressant metabolized by beta-oxidation of its heptanoic side chain, inhibits the mitochondrial oxidation of medium and short chain fatty acids in mice.
Once inside the mitochondria, L-carnitine releases these fatty acids and they are broken down by beta-oxidation to produce ATP or energy.
Caffeic acid and chlorogenic acid significantly inhibited fatty acid synthase, 3-hydroxy-3-methylglutaryl CoA reductase and acyl-CoA:cholesterol acyltransferase activities, while they increased fatty acid beta-oxidation activity and peroxisome proliferator-activated receptors alpha expression in the liver compared to the high-fat group.
This reduction in fatty acid oxidation was accompanied by a significant decrease in the activity of the long-chain isoform of the last enzyme involved in fatty acid beta-oxidation, 3-ketoacyl coenzyme A (CoA) thiolase activity (IC(50) of 75 nmol/L).