Most cells are sensitive to a deficiency of co-enzyme Q10 (CoQ10), an essential component of the mitochondrial electron transport chain. Deficiency has been implicated in clinical disorders such as heart failure, hypertension, Parkinson’s disease and obesity. While lipid lowering statin drugs inhibit the conversion of HMG-CoA to mevalonate and lowers plasma CoQ10 concentrations, CoQ10 supplementation improves the pathophysiological condition of statin therapy. Evidence suggests that CoQ10 supplementation may be useful for the treatment of obesity, oxidative stress, and the inflammatory process in metabolic syndrome. The anti-inflammatory response and lipid metabolizing effect of CoQ10 is probably mediated by transcriptional regulation of inflammation and lipid metabolism. CoQ10 has proven potential as an antioxidant molecule with anti-inflammatory properties. Recent evidence also suggests that CoQ10 may serve as adenosine monophosphate activated protein kinase (AMPK) and peroxisome proliferator activated receptors (PPARs) activators and increases the fat burning capacity of cells.
Alam A, Rahman M. Mitochondrial dysfunction in obesity: potential benefit and mechanism of C0-enzyme Q10 supplementation in metabolic syndrome. J. of Diabetes & Metabolic Disorders 2014, 13:60