More and more, researchers, clinicians, and scientists are discovering that mitochondrial dysfunction correlates with metabolic syndromes such as diabetes, specifically type 2 diabetes. While combating obesity through diet and lifestyle changes is at the forefront of solutions to address the increase in prevalence of metabolic syndrome, therapeutic interventions may be necessary to address the disease as well. Among the potential therapeutic interventions is MitoQ, a potent antioxidant directed toward the mitochondria.
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“Metabolic syndrome is associated with oxidative stress and mitochondrial dysfunction,” commented Dr. Tanecia Mitchell and Dr. Victor Darley-Usmar, both of the University of Alabama at Birmingham, in an article entitled, “Metabolic Syndrome and Mitochondrial Dysfunction: Insights from Pre-clinical Studies with a Mitochondrially Targeted Antioxidant,” which was published in Free Radical Biology and Medicine.
The two researchers were interested in a previous pre-clinical study (“The Mitochondria-targeted Antioxidant MitoQ Decreases Features of the Metabolic Syndrome in ATM+/−/ApoE−/− Mice“) that used MitoQ to fight metabolic syndrome in genetically engineered mice that demonstrated characteristics of cardiovascular pathology. The animal model was especially relevant because this mouse type develops symptoms of metabolic disorder similar to humans when the mice are fed a high fat diet.
Looking into how MitoQ could improve mitochondrial function and alter metabolic syndrome, the research team administered MitoQ to the susceptible mice. Fourteen weeks of MitoQ treatment was adequate to suppress weight gain and fat accumulation in the genetically engineered mice. The mice had more efficient carbohydrate utilization and improved their glucose and insulin levels. These results give reason to hypothesize that suppressing oxidative damage in individuals susceptible to type 2 diabetes will benefit from metabolic changes mediated by MitoQ.
It may someday be possible to use MitoQ to help stave off metabolic syndromes such as type 2 diabetes. Stated Dr. Mitchell and Dr. Darley-Usmar, “MitoQ is well tolerated in human subjects which makes it an ideal candidate to explore further in treating metabolic syndrome.” While it is not completely known how MitoQ suppresses a high level of oxidative damage, researchers are advancing their understanding of the mechanisms behind the benefits. “We look forward in anticipation to new insights into the emerging role of bioenergentic dysfunction in the cardiometabolic syndrome,” concluded Dr. Mitchell and Dr. Darley-Usmar.
