Can correction of sub-optimal coenzyme Q status improve beta-cell function in type II diabetics?

A stimulus to mitochondrial respiratory activity is a crucial component of the signal transduction mechanism whereby increased plasma glucose evokes insulin secretion by beta-cells. Efficient function of the glycerol-3-phosphate shuttle is important in this regard, and the rate-limiting enzyme in this shuttle--the mitochondrial glycerol-3-phosphate dehydrogenase (G3PD)--is underexpressed in the beta cells of human type II diabetics as well of rodents that are models for this disorder. Suboptimal tissue levels of coenzyme Q10 (CoQ) could be expected to further impair G3PD activity. Clinical reports from Japan suggest that supplemental CoQ may often improve beta-cell function and glycemic control in type II diabetics. Thus, it is proposed that correction of suboptimal CoQ status, by aiding the efficiency of G3PD and of respiratory chain function, will improve the glucose-stimulated insulin secretion of diabetic beta-cells.