June 2015
Qiuhua Shen and Janet D. Pierce

 

Abstract

Type 2 diabetes mellitus (T2DM) is a major cause of morbidity and mortality with ever increasing prevalence in the United States and worldwide. There is growing body of evidence suggesting that mitochondrial dysfunction secondary to oxidative stress plays a critical role in the pathogenesis of T2DM.

Coenzyme Q10 is an important micronutrient acting on the electron transport chain of the mitochondria with two major functions: (1) synthesis of adenosine triphosphate (ATP); and (2) a potent antioxidant. Deficiency in coenzyme Q10 is often seen in patients with T2DM. Whether restoration of coenzyme Q10 will help alleviate oxidative stress, preserve mitochondrial function, and thus improve glycemic control in T2DM is unclear.

This article reviews the relationships among oxidative stress, mitochondrial dysfunction, and T2DM and examines the evidence for potential use of coenzyme Q10 as a supplement for the treatment of T2DM.

 

Conclusion

It is clear that mitochondrial dysfunction secondary to oxidative stress contributes to the pathogenesis of T2DM. Deficiency in CoQ10 is often present among patients with T2DM due to various reasons.

As a potent antioxidant, CoQ10 is assumed to scavenge excessive ROS and provide protection to cells, especially mitochondria from oxidative damage. Therefore, restoration of CoQ10 level among patients with T2DM by supplementation of exogenous CoQ10 could potentially alleviate oxidative stress, preserve mitochondrial function, and eventually lead to improvement of glycemic control. This hypothesis was partially supported by several studies [9,10,38,39,43,44,46,47,48].

However, there were also studies that report no significant improvement in T2DM [30,41,42,45]. Thus, it is still unclear, or impossible to make a definitive conclusion on whether supplementation of CoQ10 would provide beneficial effects for patients with T2DM with current available evidence.

Large randomized clinical trials are needed to further investigate its effects in T2DM, using ubiquinol (the reduced form of CoQ10) with higher dosage.