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    Microvascular Endothelial Dysfunction in Sedentary, Obese Humans Is Mediated by NADPH Oxidase Influence of Exercise Training

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    Author
    La Favor, Justin D.; Dubis, Gabriel S.; Yan, Huimin; White, Joseph D.; Nelson, Margaret A.M.; Anderson, Ethan J.; Hickner, Robert C.
    Abstract
    Objective—The objectives of this study were to determine the impact of in vivo reactive oxygen species (ROS) on microvascular endothelial function in obese human subjects and the efficacy of an aerobic exercise intervention on alleviating obesity-associated dysfunctionality. Approach and Results—Young, sedentary men and women were divided into lean (body mass index 18–25; n=14), intermediate (body mass index 28–32.5; n=13), and obese (body mass index 33–40; n=15) groups. A novel microdialysis technique was utilized to detect elevated interstitial hydrogen peroxide (H2 O2 ) and superoxide levels in the vastus lateralis of obese compared with both lean and intermediate subjects. Nutritive blood flow was monitored in the vastus lateralis via the microdialysis-ethanol technique. A decrement in acetylcholine-stimulated blood flow revealed impaired microvascular endothelial function in the obese subjects. Perfusion of apocynin, an NADPH oxidase inhibitor, lowered (normalized) H2 O2 and superoxide levels, and reversed microvascular endothelial dysfunction in obese subjects. After 8 weeks of exercise, H2 O2 levels were decreased in the obese subjects and microvascular endothelial function in these subjects was restored to levels similar to lean subjects. Skeletal muscle protein expression of the NADPH oxidase subunits p22phox, p47phox, and p67phox was increased in obese relative to lean subjects, where p22phox and p67phox expression was attenuated by exercise training in obese subjects. Conclusions—This study implicates NADPH oxidase as a source of excessive ROS production in skeletal muscle of obese individuals and links excessive NADPH oxidase–derived ROS to microvascular endothelial dysfunction in obesity. Furthermore, aerobic exercise training proved to be an effective strategy for alleviating these maladi
    URI
    http://hdl.handle.net/10342/8217
    Subject
    acetylcholine hydrogen peroxide microdialysis obesity superoxide
    Date
    2016
    Citation:
    APA:
    La Favor, Justin D., & Dubis, Gabriel S., & Yan, Huimin, & White, Joseph D., & Nelson, Margaret A.M., & Anderson, Ethan J., & Hickner, Robert C.. (January 2016). Microvascular Endothelial Dysfunction in Sedentary, Obese Humans Is Mediated by NADPH Oxidase Influence of Exercise Training. Arteriosclerosis, Thrombosis, and Vascular Biology, (36:12), p.. Retrieved from http://hdl.handle.net/10342/8217

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    MLA:
    La Favor, Justin D., and Dubis, Gabriel S., and Yan, Huimin, and White, Joseph D., and Nelson, Margaret A.M., and Anderson, Ethan J., and Hickner, Robert C.. "Microvascular Endothelial Dysfunction in Sedentary, Obese Humans Is Mediated by NADPH Oxidase Influence of Exercise Training". Arteriosclerosis, Thrombosis, and Vascular Biology. 36:12. (.), January 2016. August 11, 2022. http://hdl.handle.net/10342/8217.
    Chicago:
    La Favor, Justin D. and Dubis, Gabriel S. and Yan, Huimin and White, Joseph D. and Nelson, Margaret A.M. and Anderson, Ethan J. and Hickner, Robert C., "Microvascular Endothelial Dysfunction in Sedentary, Obese Humans Is Mediated by NADPH Oxidase Influence of Exercise Training," Arteriosclerosis, Thrombosis, and Vascular Biology 36, no. 12 (January 2016), http://hdl.handle.net/10342/8217 (accessed August 11, 2022).
    AMA:
    La Favor, Justin D., Dubis, Gabriel S., Yan, Huimin, White, Joseph D., Nelson, Margaret A.M., Anderson, Ethan J., Hickner, Robert C.. Microvascular Endothelial Dysfunction in Sedentary, Obese Humans Is Mediated by NADPH Oxidase Influence of Exercise Training. Arteriosclerosis, Thrombosis, and Vascular Biology. January 2016; 36(12) . http://hdl.handle.net/10342/8217. Accessed August 11, 2022.
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