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We investigate whether physical activity initiated with the start of high-fat feeding would primordially prevent development
of endothelial dysfunction, and if it does, then to determine some potential mechanisms. C57BL/6 female mice were
randomly divided into three groups: 1) control low-fat diet (LF-SED; 15% of calories from fat), 2) high-fat diet (HF-SED; 45%
of calories from fat), and 3) HF diet given access to a voluntary running wheel (HF-RUN). Our hypothesis was that HF-RUN
would differ in multiple markers of endothelial dysfunction from HF-SED after 10 weeks of 45%-fat-diet, but would did not differ
from LF-SED. HF-RUN differed from HF-SED in nine determinations in which HF-SED either had decreases in 1) Acetylcholine
(ACh)-induced and flow-induced vasodilations in isolated, pressurized coronary arterioles, 2) heart phosphorylated endothelial
nitric oxide synthase (p-eNOS/eNOS) protein, 3) coronary arteriole leptin (ob) receptor protein, 4) phosphorylated signal
transducer and activator of transcription 3 (p-STAT3/STAT3) protein, and 5) coronary arteriole superoxide dismutase 1 protein;
or had increases in 6) % body fat, 7) serum leptin, 8) coronary arteriole suppressor of cytokine signaling 3 (SOCS3) protein,
and 9) coronary arteriole gp91phox protein. Higher endothelium dependent-vasodilation by ACh or leptin was abolished with
incubation of NOS inhibitor NG-nitro-L-arginine-methyl ester (L-NAME) in LF-SED and HF-RUN groups. Further, impaired
ACh-induced vasodilation in HF-SED was normalized by apocynin or TEMPOL to LF-SED and HF-RUN. These findings
demonstrate multiple mechanisms (eNOS, leptin and redox balance) by which voluntary running opposes the development of
impaired coronary arteriolar vasodilation during simultaneous high-fat feeding.
Yoonjung Park is currently an Assistant Professor in the Department of Health, Exercise and Sports Science at the Texas Tech University. He received
Ph.D. degree in Cardiovascular Exercise Physiology from Texas A&M University in the department of Health and Kinesiology and completed his
postdoctoral training in the Departments of Internal Medicine, Division of Cardiovascular Medicine, at University of Missouri. He has a number of
publications in the field of obesity, diabetes, aging and cardiovascular disease, especially microcirculation, and has an expertise in the effects of
exercise/physical activity on vascular function.
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