Paul W. Hruz, M.D., Ph.D.

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Associate Professor of Pediatrics, Endocrinology and Diabetes
Associate Professor of Pediatrics, Cell Biology & Physiology
Cell Biology & PhysiologyEndocrinology and Diabetes

phone: (314) 454-6051

Research Interests

Dr. Hruz's research interests include intermediary carbohydrate metabolism, glucose transporter structure and function and mechanism of insulin action. Currently, the mechanism(s) by which HIV protease inhibitors cause serious adverse metabolic effects including peripheral lipoatrophy, visceral adiposity, hypertriglyceridemia, and insulin resistance are being investigated. The laboratory has discovered that HIV protease inhibitors selectively and reversibly inhibit the GLUT4 facilitative glucose transporter. Ongoing studies are being directed toward elucidating the selectivity of these drugs in blocking the activity of each of the known facilitative glucose transport proteins. The tertiary structure of the facilitative glucose transporters is also being investigated using state-of-the-art biophysical approaches.


  • BS, Marquette University1987
  • PhD, Medical College of Wisconsin1993
  • MD, Medical College of Wisconsin1994


  • Pediatric Residency, University of Washington1994 - 1997
  • Pediatric Endocrinology Fellowship, Washington University1997 - 2000
  • Certification in Healthcare Ethics, National Catholic Bioethics Center2017

Licensure and Board Certification

  • 1997 - PresBoard Certified in General Pediatrics
  • 2000 - PresMO, Stae License
  • 2001 - PresBoard Certified in Pediatric Endocrinology & Metabolism

Honors and Awards

  • National Institute of Chemists Research and Recognition Award1987
  • Phi Beta Kappa1987
  • Phi Lambda Upsilon (Honorary Chemical Society)1987
  • American Heart Association Predoctoral Fellowship Award1988
  • Alpha Omega Alpha1994
  • Armond J. Quick Award for Excellence in Biochemistry1994
  • NIDDK/Diabetes Branch Most Outstanding Resident1994
  • Pfizer Postdoctoral Fellowship Award1998
  • Scholar, Child Health Research Center of Excellence in Developmental Biology at Washington University2002
  • Julio V Santiago, M.D. Scholar in Pediatrics2013
  • Redemptor Hominis Award for Outstanding Contributions to the Study of Bioethics2017
  • Eli Lilly Outstanding Contribution to Drug Discovery: Emerging Biology Award2018
  • Scholar-Innovator Award, Harrington Discovery Institute2018
  • Linacre Award2021

Selected Publications view all (52)

Publication Co-Authors

Mammalian Glucose Transporter Activity is Dependent upon Anionic and Conical Phospholipids. J Biol Chem. 2016. doi:10.1074/jbc.M116.730168  PMID:27302065 
Trehalose inhibits solute carrier 2A (SLC2A) proteins to induce autophagy and prevent hepatic steatosis. Sci Signal. 2016;9(416):ra21. doi:10.1126/scisignal.aac5472  PMID:26905426 
The Glucose Transporter PfHT1 Is an Antimalarial Target of the HIV Protease Inhibitor Lopinavir. Antimicrob Agents Chemother. 2015;59(10):6203-9. doi:10.1128/AAC.00899-15  PMCID:PMC4576095  PMID:26248369 
Expression, purification, and functional characterization of the insulin-responsive facilitative glucose transporter GLUT4. Protein Sci. 2015. doi:10.1002/pro.2812  PMID:26402434 
In Silico Modeling-based Identification of Glucose Transporter 4 (GLUT4)-selective Inhibitors for Cancer Therapy. J Biol Chem. 2015;290(23):14441-53. doi:10.1074/jbc.M114.628826  PMID:25847249 
Isoform-selective inhibition of facilitative glucose transporters: elucidation of the molecular mechanism of HIV protease inhibitor binding. J Biol Chem. 2014;289(23):16100-16113. doi:10.1074/jbc.M113.528430  PMCID:PMC4047383  PMID:24706759 
Saxagliptin Improves Glucose Tolerance but not Survival in a Murine Model of Dilated Cardiomyopathy. Cardiovasc Endocrinol. 2012;1(4):74-82. doi:10.1097/XCE.0b013e32835bfb24  PMCID:PMC3686315  PMID:23795310 
GLUT4, GLUT1, and GLUT8 are the dominant GLUT transcripts expressed in the murine left ventricle. Cardiovasc Diabetol. 2012;11:63. doi:10.1186/1475-2840-11-63  PMCID:PMC3416696  PMID:22681646 
Acute sulfonylurea therapy at disease onset can cause permanent remission of KATP-induced diabetes. Diabetes. 2011;60(10):2515-22. doi:10.2337/db11-0538  PMCID:PMC3178299  PMID:21813803 
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