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J Diabetes Metab Disord. 2014 May 23;13:60. doi: 10.1186/2251-6581-13-60. eCollection 2014.

Mitochondrial dysfunction in obesity: potential benefit and mechanism of Co-enzyme Q10 supplementation in metabolic syndrome.

Author information

1
School of Biomedical Science, The University of Queensland, Brisbane, Australia ; Department of Pharmaceutical Sciences, North South University, Dhaka, Bangladesh.
2
Department of Pharmaceutical Sciences, North South University, Dhaka, Bangladesh.

Abstract

Co-enzyme Q10 (Co-Q10) is an essential component of the mitochondrial electron transport chain. Most cells are sensitive to co-enzyme Q10 (Co-Q10) deficiency. This deficiency has been implicated in several clinical disorders such as heart failure, hypertension, Parkinson's disease and obesity. The lipid lowering drug statin inhibits conversion of HMG-CoA to mevalonate and lowers plasma Co-Q10 concentrations. However, supplementation with Co-Q10 improves the pathophysiological condition of statin therapy. Recent evidence suggests that Co-Q10 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 Co-Q10 is probably mediated by transcriptional regulation of inflammation and lipid metabolism. This paper reviews the evidence showing beneficial role of Co-Q10 supplementation and its potential mechanism of action on contributing factors of metabolic and cardiovascular complications.

KEYWORDS:

Co-enzyme Q10; Inflammation; Metabolic syndrome; Obesity; Oxidative stress

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