Coenzyme Q10, Glucose Homeostasis and the Probable Mediating Role of Adipokines

Abstract

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.
6-8
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.11
This 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.