Sung Hee Um
Sung Hee Um PhD
Professor: Graduate Program, Research Area, Laboratory, E-mail, Tel
Graduate Program Metabolic & Genetic Disease
Research Area Metabolism, Diabetes, Obesity
Laboratory Metabolic Diseases Lab Laboratory
Tel +82-31-299-6123
Education & Careers
  • 1994: B.S. Department of Pharmacy, Sungkyunkwan University
    1996: M.S. School of Pharmacy, Sungkyunkwan University
    2004 Ph.D. Friedrich Miescher Institute for Biomedical Research, University of Basel, Switzerland
    2004 - 2009: Postdoctoral Fellow, College of Medicine, University of Cincinnati, U.S.A
    2009 - present: Professor, Department of Molecular Cell Biology, Sungkyunkwan University, School of Medicine, Korea
Research Interest
The main pathological features common to obesity and diabetes are the deregulation of nutrient and energy homeostasis. Studying the signaling pathways involved in nutrient and energy homeostasis could lead to better understanding of pathophysiology of metabolic disorders. We are interested in understanding how cells sense and integrate signals from growth factors and from nutrients to mediate metabolic responses, and how such signaling pathway is deregulated in pathological conditions. Integrating the use of biochemistry, molecular biology, mouse model and patient samples, we aim to define deregulation of signaling pathway that may lead to impairment of nutrient and energy homeostasis. This body of work will provide a physiological basis to identify molecular targets with great potential value in the development of therapeutic strategies to treat metabolic disorders. Sung Hee Um was awarded TJ Park Science Fellowship from POSCO TJ Park foundation, and a grant from Samsung science & technology Foundation.
Representative Research Achievements
  • 1)Kim HJ*, Lee DE*, Park EC, Ra M-J, Jung S-M, Yu J-M, Um SH**, and Kim KH**(* equally contributed) (**corresponding author),, 2022: Anti-Adipogenic Effects of Salicortin from the Twigs of Weeping Willow (Salix pseudolasiogyne) in 3T3-L1 Cells. Molecules. 27(20), 6954

    2) Seo DS, Chau GC, Baek KH, Um SH*, 2019: A single extra copy of Down syndrome critical region 1-4 results in impaired hepatic glucose homeostasis. Mol Metab., 21, 82-89

    3) Chau GC,* Im DU,* Kang TM, Bae JM, Won Kim, Pyo SN, Moon EY, and Um SH ** (*equally contribution), 2017: mTOR controls ChREBP transcriptional activity and pancreatic β cell survival under diabetic stress. J. Cell Biol., 216(7), 2091-2105

    4) Um SH*, Sticker JM, Chau GC, Vintersten K, Mueller M, Gangliff YG, Adams RH, Spetz JF, Elghazi L, Tsch&246p MH, Thomas G and Kozma SC*. 2015: S6K1-mediated pancreatic b-cell size is independent of intrauterine growth restriction. J Clin Invest. 2015 Jul 1125(7):2736-47

    5) Kim KJ, Pyo S, Um SH*, 2012: S6K2 deficiency enhances ketone body production and increases PPARα activity in the liver. Hepatology 2012 Jun 55(6):1727-37