Grew up in Seattle. WA. Avid Seahawks fan. Avid fan of the outdoors. BYU graduate in global public health. Junior scientist with plans to attend medical school. Interested in pediatrics and research. Potentially interested in the fields of gastroenterology, endocrinology, global health or sports medicine. Fascinated by interdisciplinary approaches to solving global medical issues. Interested in joint MD programs. Currently an LSRP in the Sellers lab at Stanford University. Technical skills include working with mouse models, intestinal perfusion surgeries and qPCR. Interested in learning more techniques and expanding my knowledge and exposure in the field of medicine.

Current Role at Stanford

Life Science Research Professional

Education & Certifications

  • BS, Brigham Young University, Global Public Health (2016)


All Publications

  • High-Mobility Group Box 1 Disrupts Metabolic Function with Cigarette Smoke Exposure in a Ceramide-Dependent Manner INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Taylor, O. J., Thatcher, M. O., Carr, S. T., Gibbs, J. L., Trumbull, A. M., Harrison, M. E., Winden, D. R., Pearson, M. J., Tippetts, T. S., Holland, W. L., Reynolds, P. R., Bikman, B. T. 2017; 18 (5)


    We have previously found that cigarette smoke disrupts metabolic function, in part, by increasing muscle ceramide accrual. To further our understanding of this, we sought to determine the role of the cytokine high-mobility group box 1 (HMGB1), which is increased with smoke exposure, in smoke-induced muscle metabolic perturbations. To test this theory, we determined HMGB1 from lungs of human smokers, as well as from lung cells from mice exposed to cigarette smoke. We also treated cells and mice directly with HMGB1, in the presence or absence of myriocin, an inhibitor of serine palmitoyltransferase, the rate-limiting enzyme in ceramide biosynthesis. Outcomes included assessments of insulin resistance and muscle mitochondrial function. HMGB1 was significantly increased in both human lungs and rodent alveolar macrophages. Further testing revealed that HMGB1 treatment elicited a widespread increase in ceramide species and reduction in myotube mitochondrial respiration, an increase in reactive oxygen species, and reduced insulin-stimulated Akt phosphorylation. Inhibition of ceramide biosynthesis with myriocin was protective. In mice, by comparing treatments of HMGB1 injections with or without myriocin, we found that HMGB1 injections resulted in increased muscle ceramides, especially C16 and C24, which were necessary for reduced muscle mitochondrial respiration and compromised insulin and glucose tolerance. In conclusion, HMGB1 may be a necessary intermediate in the ceramide-dependent metabolic consequences of cigarette smoke exposure.

    View details for DOI 10.3390/ijms18051099

    View details for Web of Science ID 000404113900201

    View details for PubMedID 28531105

    View details for PubMedCentralID PMC5455007

  • LIPOPOLYSACCHARIDE DISRUPTS MITOCHONDRIAL PHYSIOLOGY IN SKELETAL MUSCLE VIA DISPARATE EFFECTS ON SPHINGOLIPID METABOLISM SHOCK Hansen, M. E., Simmons, K. J., Tippetts, T. S., Thatcher, M. O., Saito, R. R., Hubbard, S. T., Trumbull, A. M., Parker, B. A., Taylor, O. J., Bikman, B. T. 2015; 44 (6): 585–92


    Lipopolysaccharides (LPS) are prevalent pathogenic molecules that are found within tissues and blood. Elevated circulating LPS is a feature of obesity and sepsis, both of which are associated with mitochondrial abnormalities that are key pathological features of LPS excess. However, the mechanism of LPS-induced mitochondrial alterations remains poorly understood. Herein we demonstrate the necessity of sphingolipid accrual in mediating altered mitochondrial physiology in skeletal muscle following LPS exposure. In particular, we found LPS elicited disparate effects on the sphingolipids dihydroceramides (DhCer) and ceramides (Cer) in both cultured myotubes and in muscle of LPS-injected mice. Although LPS-treated myotubes had reduced DhCer and increased Cer as well as increased mitochondrial respiration, muscle from LPS-injected mice manifested a reverse trend, namely elevated DhCer, but reduced Cer as well as reduced mitochondrial respiration. In addition, we found that LPS treatment caused mitochondrial fission, likely via dynamin-related protein 1, and increased oxidative stress. However, inhibition of de novo sphingolipid biosynthesis via myriocin protected normal mitochondrial function in spite of LPS, but inhibition of DhCer desaturase 1, which increases DhCer, but not Cer, exacerbated mitochondrial respiration with LPS. In an attempt to reconcile the incongruent effects of LPS in isolated muscle cells and whole muscle tissue, we incubated myotubes with conditioned medium from treated macrophages. In contrast to direct myotube LPS treatment, conditioned medium from LPS-treated macrophages reduced myotube respiration, but this was again mitigated with sphingolipid inhibition. Thus, macrophage sphingolipid production appears to be necessary for LPS-induced mitochondrial alterations in skeletal muscle tissue.

    View details for DOI 10.1097/SHK.0000000000000468

    View details for Web of Science ID 000365673700011

    View details for PubMedID 26529656

    View details for PubMedCentralID PMC4851226

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