Browsing by Author "Choi, Yeon-Kyung"

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    PDK4 Augments ER–Mitochondria Contact to Dampen Skeletal Muscle Insulin Signaling During Obesity
    (American Diabetes Association, 2019-03) Thoudam, Themis; Ha, Chae-Myeong; Leem, Jaechan; Chanda, Dipanjan; Park, Jong-Seok; Kim, Hyo-Jeong; Jeon, Jae-Han; Choi, Yeon-Kyung; Liangpunsakul, Suthat; Huh, Yang Hoon; Kwon, Tae-Hwan; Park, Keun-Gyu; Harris, Robert A.; Park, Kyu-Sang; Rhee, Hyun-Woo; Lee, In-Kyu; Medicine, School of Medicine
    Background: Recent evidence in mobile health has demonstrated that, in some cases, apps are an effective way to improve health care delivery. Health care interventions delivered via mobile technology have demonstrated both practicality and affordability. Lately, cognitive behavioral therapy (CBT) interventions delivered over the internet have also shown a meaningful impact on patients with anxiety and depression. Objective: Given the growing proliferation of smartphones and the trust in apps to support improved health behaviors and outcomes, we were interested in comparing a mobile app with Web-based methods for the delivery of CBT. This study aimed to compare the usability of a CBT mobile app called MoodTrainer with an evidence-based website called MoodGYM. Methods: We used convenience sampling to recruit 30 students from a large Midwestern university and randomly assigned them to either the MoodGYM or MoodTrainer user group. The trial period ran for 2 weeks, after which the students completed a self-assessment survey based on Nielsen heuristics. Statistical analysis was performed to compare the survey results from the 2 groups. We also compared the number of modules attempted or completed and the time spent on CBT strategies. Results: The results indicate that the MoodTrainer app received a higher usability score when compared with MoodGYM. Overall, 87% (13/15) of the participants felt that it was easy to navigate through the MoodTrainer app compared with 80% (12/15) of the MoodGYM participants. All MoodTrainer participants agreed that the app was easy to use and did not require any external assistance, whereas only 67% (10/15) had the same opinion for MoodGYM. Furthermore, 67% (10/15) of the MoodTrainer participants found that the navigation controls were easy to locate compared with 80% (12/15) of the MoodGYM participants. MoodTrainer users, on average, completed 2.5 modules compared with 1 module completed by MoodGYM users. Conclusions: As among the first studies to directly compare the usability of a mobile app-based CBT with smartphone-specific features against a Web-based CBT, there is an opportunity for app-based CBT as, at least in our limited trial, it was more usable and engaging. The study was limited to evaluate usability only and not the clinical effectiveness of the app.
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    Pyruvate Dehydrogenase Kinase Is a Metabolic Checkpoint for Polarization of Macrophages to the M1 Phenotype
    (Frontiers, 2019-05-07) Min, Byong-Keol; Park, Sungmi; Kang, Hyeon-Ji; Kim, Dong Wook; Ham, Hye Jin; Ha, Chae-Myeong; Choi, Byung-Jun; Lee, Jung Yi; Oh, Chang Joo; Yoo, Eun Kyung; Kim, Hui Eon; Kim, Byung-Gyu; Jeon, Jae-Han; Hyeon, Do Young; Hwang, Daehee; Kim, Yong-Hoon; Lee, Chul-Ho; Lee, Taeho; Kim, Jung-whan; Choi, Yeon-Kyung; Park, Keun-Gyu; Chawla, Ajay; Lee, Jongsoon; Harris, Robert A.; Lee, In-Kyu; Biochemistry and Molecular Biology, School of Medicine
    Metabolic reprogramming during macrophage polarization supports the effector functions of these cells in health and disease. Here, we demonstrate that pyruvate dehydrogenase kinase (PDK), which inhibits the pyruvate dehydrogenase-mediated conversion of cytosolic pyruvate to mitochondrial acetyl-CoA, functions as a metabolic checkpoint in M1 macrophages. Polarization was not prevented by PDK2 or PDK4 deletion but was fully prevented by the combined deletion of PDK2 and PDK4; this lack of polarization was correlated with improved mitochondrial respiration and rewiring of metabolic breaks that are characterized by increased glycolytic intermediates and reduced metabolites in the TCA cycle. Genetic deletion or pharmacological inhibition of PDK2/4 prevents polarization of macrophages to the M1 phenotype in response to inflammatory stimuli (lipopolysaccharide plus IFN-γ). Transplantation of PDK2/4-deficient bone marrow into irradiated wild-type mice to produce mice with PDK2/4-deficient myeloid cells prevented M1 polarization, reduced obesity-associated insulin resistance, and ameliorated adipose tissue inflammation. A novel, pharmacological PDK inhibitor, KPLH1130, improved high-fat diet-induced insulin resistance; this was correlated with a reduction in the levels of pro-inflammatory markers and improved mitochondrial function. These studies identify PDK2/4 as a metabolic checkpoint for M1 phenotype polarization of macrophages, which could potentially be exploited as a novel therapeutic target for obesity-associated metabolic disorders and other inflammatory conditions.