Coenzyme Q10 is one of the most popular nutritional supplements, which has been discovered in 1955. It is also known as ubiquinone, Q10, CoQ and vitamin Q10. This coenzyme has two isoforms; the oxidized form, ubiquinone, is an electron carrier in mitochondrial respiratory chain and the reduced form, ubiquinol, acts as an antioxidant.1,2 Studies reported its beneficial effects in some diseases such as diabetes, heart failure, hypertension, and Parkinson disease. 3,4 Q10 has also been proposed to be helpful in prevention and treatment of neurodegenerative and mitochondrial related diseases.5 Q10 could potentially be effective on metabolic disorders including lipid profile, blood pressure, glycemic control and insulin resistance in different diseases. [6][7][8] Many diseases are accompanied with imapired glycemic control and insulin resistance.9 Phosphorylation of Insulin Receptor Substrates (IRS) is crucial for insulin signalling cascade, which in turn activates the mitogen-activated protein kinase (MAP-Kinase) with major mitogenic effects and phosphatidylinositol-3-Kinase (PI-3K) with prominent metabolic properties including appropriate cellular glucose distribution.10 Coenzyme Q10 might induce the tyrosine kinase and phosphatidylinositol 3 kinase (PI3k) activity in liver. These enzymes are involved in improving insulin cascade and increasing GLUT2 and tyrosine phosphorylation of IRS-1, which could in turn enhance glucose uptake and inhibit gluconeogenesis in liver.
11This antioxidant has been shown to reduce HbA1C levels in experimental and clinical studies and to improve long term glycemic control. 6,7,12,13 It could also increase insulin production and secretion probably by stimulating ATP generation in pancreatic beta cells.14 Other proposed mechanisms include regulation of insulin receptors, glucose transporters, lipid profile, redox system, and receptors of advanced glycated end products. 15 Obesity, the major growing health problem worldwide, is one the most important contributors of initiation and progression of insulin resistance. 16 The potential mechanisms include higher production of fatty acids, activation of Toll-like receptor 4 and the innate immune system, alterations in endocrine and inflammatory mediators and activation of nuclear factor-κB (NF-κB).
17Recently the metabolic functions of adipose derived peptides, adipokines, have been investigated progressively in different disorders. The changes in the secretion of adipokines in obesity could inhibit insulin signalling through increasing inflammatory adipocytokines and other mediators interfering the IRS phosphorylation and integrity. 17 The relationship between the major adipokines, leptin, adiponectin, resistin and visfatin with glucose homeostasis has previously been demonstrated. 18,19 Leptin could contribute to glucose homeostasis through direct and indirect actions on peripheral tissues. Direct leptin actions might inhibit insulin and glucagon secretion from pancreatic cells. Moreover, leptin could potentially affect insulin signaling in a...