Physical Activity Opposes Coronary Vascular Dysfunction In High Fat Feeding-induced Obese Mice | 6419
ISSN: 2165-7904

Journal of Obesity & Weight Loss Therapy
Open Access

Our Group organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations
700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)

Physical activity opposes coronary vascular dysfunction in high fat feeding-induced obese mice

International Conference and Exhibition on Obesity & Weight Management

Yoonjung Park

ScientificTracks Abstracts: J Obes Wt Loss Ther

DOI: 10.4172/2165-7904.S1.002

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.