Bio

Kate Turk, MD is a resident physician in Pediatrics at Stanford University School of Medicine. Her academic interests center on sustainable pediatric global health, health policy, and innovative public health technology.

Dr. Turk is part of Stanford’s Global Health Scholarly Concentration and is focused on the development of scalable, evidence-based interventions to improve pediatric outcomes in resource-limited settings. Her current project is based in Cusco, Peru, in collaboration with the Cusco Ministry of Health, EsSalud network, and local clinical partners, and aims to strengthen frontline pediatric provider capacity, including the implementation and evaluation of digital clinical decision support tools and educational platforms, across the province of Cusco. Some of her prior global health projects have included developing a curriculum to improve stroke prevention education in Huaral, Peru and partnering with Global Brigades Inc. to improve access to regular medical care, clean water, and public health infrastructure within Nicaragua and Panama. She was recognized as Stanford’s 2025-2026 Zlotnick Global Health Scholar.

Additional projects include working with the Washington State legislature and Department of Health to implement prescription label translation in pharmacies across the state, organizing a 6-part lecture series focused on teaching advocacy and community organizing techniques using the lens of food insecurity to California-based pediatrics residents, and leading/participating in various groups focused on mentorship for students underrepresented in medicine, language justice, and global health.

Dr. Turk received her medical degree from the University of Washington School of Medicine (UWOSM), where she developed a strong foundation in clinical care and a commitment to health equity. At the UWSOM, she completed the Latinx Health and Global Health pathways, and graduated with Alpha Omega Alpha honors.

Clinical Focus

  • Residency
  • Pediatrics
  • Global Health
  • Health Policy

Professional Education

  • MD, University of Washington, Medicine (2024)
  • BS, University of Washington, Biology (Physiology) (2018)

All Publications

  • Comparison between genetic and pharmaceutical disruption of Ldlr expression for the development of atherosclerosis. Journal of lipid research Gomes, D., Wang, S., Goodspeed, L., Turk, K. E., Wietecha, T., Liu, Y., Bornfeldt, K. E., O'Brien, K. D., Chait, A., den Hartigh, L. J. 2022; 63 (3): 100174

    Abstract

    Antisense oligonucleotides (ASOs) against Ldl receptor (Ldlr-ASO) represent a promising strategy to promote hypercholesterolemic atherosclerosis in animal models without the need for complex breeding strategies. Here, we sought to characterize and contrast atherosclerosis in mice given Ldlr-ASO with those bearing genetic Ldlr deficiency. To promote atherosclerosis, male and female C57Bl6/J mice were either given weekly injections of Ldlr-ASO (5 mg/kg once per week) or genetically deficient in Ldlr (Ldlr-/-). Mice consumed either standard rodent chow or a diet high in saturated fat and sucrose with 0.15% added cholesterol for 16 weeks. While both models of Ldlr deficiency promoted hypercholesterolemia, Ldlr-/- mice exhibited nearly 2-fold higher cholesterol levels than Ldlr-ASO mice, reflected by increased VLDL and LDL levels. Consistent with this, the en face atherosclerotic lesion area was 3-fold and 3.6-fold greater in male and female mice with genetic Ldlr deficiency, respectively, as compared with the modest atherosclerosis observed following Ldlr-ASO treatment. Aortic sinus lesion sizes, fibrosis, smooth muscle actin, and necrotic core areas were also larger in Ldlr-/- mice, suggesting a more advanced phenotype. Despite a more modest effect on hypercholesterolemia, Ldlr-ASO induced greater hepatic inflammatory gene expression, macrophage accumulation, and histological lobular inflammation than was observed in Ldlr-/- mice. We conclude Ldlr-ASO is a promising tool for the generation of complex rodent models with which to study atherosclerosis but does not promote comparable levels of hypercholesterolemia or atherosclerosis as Ldlr-/- mice and increases hepatic inflammation. Thus, genetic Ldlr deficiency may be a superior model, depending on the proposed use.

    View details for DOI 10.1016/j.jlr.2022.100174

    View details for PubMedID 35101425

    View details for PubMedCentralID PMC8953673

  • Sexually Dimorphic Relationships Among Saa3 (Serum Amyloid A3), Inflammation, and Cholesterol Metabolism Modulate Atherosclerosis in Mice. Arteriosclerosis, thrombosis, and vascular biology Chait, A., Wang, S., Goodspeed, L., Gomes, D., Turk, K. E., Wietecha, T., Tang, J., Storey, C., O'Brien, K. D., Rubinow, K. B., Tang, C., Vaisar, T., Gharib, S. A., Lusis, A. J., Den Hartigh, L. J. 2021; 41 (6): e299-e313

    Abstract

    [Figure: see text].

    View details for DOI 10.1161/ATVBAHA.121.316066

    View details for PubMedID 33761762

    View details for PubMedCentralID PMC8159856

  • Rosiglitazone Improves Insulin Resistance Mediated by 10,12 Conjugated Linoleic Acid in a Male Mouse Model of Metabolic Syndrome. Endocrinology Wang, S., Goodspeed, L., Turk, K. E., Houston, B., den Hartigh, L. J. 2017; 158 (9): 2848-2859

    Abstract

    Trans-10, cis-12 conjugated linoleic acid (10,12 CLA) is a dietary fatty acid that promotes weight loss and disproportionate fat loss. Obese mice fed a high-fat, high-sucrose (HFHS) diet containing 10,12 CLA are resistant to weight gain and contain markedly reduced subcutaneous fat and adiponectin, with a concurrent lack of improvement in insulin sensitivity despite significant weight loss. Taken together, 10,12 CLA promotes a phenotype resembling peroxisome proliferator-activated receptor (PPAR)γ antagonism. Because thiazolidinediones such as rosiglitazone (Rosi) are used clinically to improve insulin sensitivity by activating PPARγ, with particular efficacy in subcutaneous white adipose tissue, we hypothesized that Rosi would improve glucose metabolism in mice losing weight with 10,12 CLA. Obese low-density lipoprotein receptor-deficient mice were fed a HFHS control diet, or supplemented with 1% 10,12 CLA with or without Rosi (10 mg/kg) for 8 weeks. Body composition, glucose and insulin tolerance tests, tissue gene expression, and plasma lipid analyses were performed. Mice consuming 10,12 CLA with Rosi lost weight and body fat compared with control groups, but with a healthier redistribution of body fat toward more subcutaneous adipose tissue than with 10,12 CLA alone. Further, Rosi improved 10,12 CLA-mediated insulin resistance parameters and increased plasma and subcutaneous adipose tissue adiponectin levels without adverse effects on plasma or hepatic lipids. We conclude that cotreatment of mice with 10,12 CLA and Rosi promotes fat loss with a healthier fat distribution that leads to improved insulin sensitivity, suggesting that the combination treatment strategy of 10,12 CLA with Rosi could have therapeutic potential for obesity treatment.

    View details for DOI 10.1210/en.2017-00213

    View details for PubMedID 28651330

    View details for PubMedCentralID PMC5659669