Bio

Dr. Ying Zhu is a postdoctoral scholar in the Rosen Lab, Department of Pediatrics, Division of Gastroenterology, Hepatology & Nutrition at Stanford University. She earned her PhD in 2023 from the Friedman School of Nutrition Science and Policy at Tufts University. In the Rosen Lab, Dr. Zhu investigates intestinal epithelial metabolic dysfunction in pediatric inflammatory bowel diseases and chronic intestinal inflammation. Her primary objective is to characterize metabolic reprogramming in ulcerative colitis epithelium and to identify defects that persist in patient-derived organoids, or colonoids. Her broader research interests lie in the interplay between intestinal energy metabolism and epithelial barrier homeostasis in children with ulcerative colitis.

Institute Affiliations

Boards, Advisory Committees, Professional Organizations

  • Member, American Gastroenterological Association (2024 - Present)
  • Member, American Society of Nutrition (2017 - Present)

Stanford Advisors

Contact

  • Academic
    yzhu10@stanford.edu
    University - Scholar Department: Pediatrics Position: Postdoctoral Scholar

All Publications

  • Patient-derived colon epithelial organoids reveal lipid-related metabolic dysfunction in pediatric ulcerative colitis. Nature communications Ojo, B. A., Zhu, Y., Heo, L., Fox, S. R., Qiao, Y., Waddell, A., Moreno-Fernandez, M. E., Gibson, M., Tran, T., Dunn, A. L., Elknawy, E. I., Saini, N., López-Rivera, J. A., Divanovic, S., Dai, Y., de Jesus Perez, V. A., Rosen, M. J. 2025; 16 (1): 11026

    Abstract

    Ulcerative colitis (UC) is associated with epithelial metabolic derangements which exacerbate gut inflammation. Here, we develop colon organoid (colonoid) lines from pediatric patients with endoscopically active UC, inactive UC, and those without intestinal inflammation to interrogate functional metabolic differences in the colon epithelia. We demonstrate that active UC colonoids exhibit hypermetabolic features and cellular stress, specifically during differentiation. Hypermetabolism in active UC colonoids is driven, in part, by increased proton leak, and excess lipid accumulation. Active UC colonoids exhibit heightened activation of the master lipid regulator PPAR-α and its transcriptional pathways. Pharmacological PPAR-α inhibition limits lipid accumulation, induces a metabolic shift towards glucose utilization, suppresses hypermetabolism, and reduces chemokine secretion and cellular stress markers. Collectively, our findings identify lipid-related metabolic dysfunction as a key pathologic feature of the pediatric UC epithelium and highlight the potential of patient-derived colonoids as a preclinical model for evaluating epithelial-targeted therapies addressing this dysfunction.

    View details for DOI 10.1038/s41467-025-65988-2

    View details for PubMedID 41372139

    View details for PubMedCentralID PMC12695892