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Updated: Dec 23, 2025
Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry
Published on: May 5, 2022
Effect of mitoquinone (Mito-Q) on neuropathic endpoints in an obese and type 2 diabetic rat model
Brian Fink1, Lawrence Coppey2, Eric Davidson2
1Department of Veterans Affairs, Iowa City Health Care System, Iowa City, IA, USA.
Abstract:
This study sought to determine whether the addition of mitoquinone (Mito-Q) in the diet is an effective treatment for peripheral neuropathy in animal models of diet-induced obesity (pre-diabetes) and type 2 diabetes. Unlike other anti-oxidative stress compounds investigated as a treatment for peripheral neuropathy, Mito-Q specifically targets mitochondria. Although mito-Q has been shown to reduce oxidative stress generated by mitochondria there have been no studies performed of the effect of Mito-Q on peripheral neuropathy induced by diet-induced obesity or type 2 diabetes. Diet-induced obese (12 weeks after high fat diet) or type 2 diabetic rats (12 weeks of high fat diet and 4 weeks after the onset of hyperglycemia) were treated via the diet with Mito-Q (0.93 g/kg diet) for 12 weeks. Afterwards, glucose utilization, vascular reactivity of epineurial arterioles to acetylcholine and peripheral neuropathy related endpoints were examined. The addition of Mito-Q to the diets of obese and diabetic rats improved motor and/or sensory nerve conduction velocity, cornea and intraepidermal nerve fibre density, cornea sensitivity and thermal nociception. Surprisingly, treating obese and diabetic rats with Mito-Q did not improve glucose utilization or vascular reactivity by epineurial arterioles to acetylcholine. These studies imply that mitochondrial dysfunction contributes to peripheral neuropathy in animal models of pre-diabetes and late-stage type 2 diabetes. However, improvement in peripheral neuropathy following treatment with Mito-Q was not associated with improvement in glucose utilization or vascular reactivity of epineurial arterioles to acetylcholine.
Insights
Mito-Q supplementation improved peripheral neuropathy in obese and diabetic rats, enhancing nerve function and density. However, it did not improve glucose utilization or blood vessel response, suggesting mitochondrial dysfunction contributes to neuropathy independent of these factors.
Area of Science:
- Biomedical Science
- Neuroscience
- Metabolic Research
Background:
- Peripheral neuropathy is a common complication of obesity and type 2 diabetes.
- Mitochondrial dysfunction is implicated in the pathogenesis of diabetic neuropathy.
- Mito-Q, a mitochondria-targeted antioxidant, has not been previously studied for its effects on diet-induced peripheral neuropathy.
Purpose of the Study:
- To investigate the efficacy of dietary Mito-Q supplementation in treating peripheral neuropathy in animal models of diet-induced obesity and type 2 diabetes.
- To determine if Mito-Q improves nerve function, nerve density, and pain perception in these models.
- To assess the impact of Mito-Q on glucose utilization and vascular reactivity.
Main Methods:
- Diet-induced obese and type 2 diabetic rats were fed a diet supplemented with Mito-Q for 12 weeks.
- Peripheral neuropathy endpoints, including nerve conduction velocity, nerve fiber density, corneal sensitivity, and thermal nociception, were evaluated.
- Glucose utilization and vascular reactivity of epineurial arterioles were also assessed.
Main Results:
- Mito-Q treatment significantly improved motor and sensory nerve conduction velocity.
- Corneal and intraepidermal nerve fiber density, corneal sensitivity, and thermal nociception were enhanced in Mito-Q treated rats.
- Surprisingly, Mito-Q did not improve glucose utilization or vascular reactivity to acetylcholine.
Conclusions:
- Mitochondrial dysfunction plays a role in the development of peripheral neuropathy in pre-diabetic and type 2 diabetic states.
- Dietary Mito-Q effectively ameliorates peripheral neuropathy in these models, independent of improvements in glucose metabolism or vascular function.
- Targeting mitochondrial oxidative stress with Mito-Q represents a potential therapeutic strategy for diabetic peripheral neuropathy.
