H. Henry Dong, PhD
Professor of Pediatrics


Dr. Dong is a member of the Cellular and Molecular Pathology Graduate Training Program.

Office Location:
Children's Hospital of Pittsburgh of UPMC
Rangos Research Center
4401 Penn Avenue
Pittsburgh, PA 15244

Contact Information:
Office Telephone: 412-692-6324
Lab Telephone: 412-692-6570
Email: dongh@pitt.edu

Lab Address and Phone
Div. of Endocrinology and Diabetes
Dept. of Pediatrics
Children's Hospital of Pittsburgh of UPMC
University of Pittsburgh School of Medicine
4401 Penn Ave.
Pittsburgh, PA 15224

Phone 412-692-9190

Education

  • PhD - Uppsala University, Sweden, 1995

Awards and Honors

  • 2006-2011 American Diabetes Career Development Award
  • 2004-2006 American Diabetes Association Islet Cell Replacement Research Award

Research Interests

Dr. Dong is Professor in the Department of Pediatrics, University of Pittsburgh School of Medicine. Dr. Dong focuses on studies of the mechanisms underlying beta-cell failure and diabetic hypertriglyceridemia in type 2 diabetes. Type 2 diabetes results from beta-cell failure, culminating in the inability of beta-cells to compensate for insulin resistance in at-risk subjects with obesity. Beta-cell compensation is an adaptive mechanism by which beta-cells increase insulin secretion to overcome insulin resistance for maintaining euglycemia in obesity. Beta-cell compensation culminates in the expansion of beta-cell mass and/or upregulation of insulin synthesis and secretion. Failure of beta-cells to compensate for insulin resistance contributes to insulin insufficiency and overt diabetes. How beta-cells compensate for insulin resistance and what causes beta-cell failure are poorly understood. Likewise, the molecular basis that links insulin resistance to the pathogenesis of hypertriglyceridemia is incompletely understood. Diabetic hypertriglyceridemia is characterized by a triad plasma lipid profile, i.e., increased triglyceride and LDL-cholesterol levels, and decreased HDL-cholesterol levels. Diabetic hypertriglyceridemia is considered an independent risk factor for coronary artery disease. Dr. Dong's lab works to characterize factors in glucose and lipid metabolism to understand how insulin resistance perturbs carbohydrate metabolism, contributing to the development of diabetic hypertriglyceridemia. Dr. Dong's group is also positioned to identify genetic factor(s) that are responsible for coupling beta-cell compensation with overnutrition in obesity to understand the underlying mechanism of beta-cell failure in diabetes. Dr. Dong is also a faculty member of the Center for Liver Disease in the Department of Pathology of UPMC, and a faculty member for the Training Program in Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Pittsburgh School of Medicine.

Selected Publications

View Dr. Dong's publications on PubMed

  1. Altomonte, J., Cong, L., Richter, A., Harbaran, S., Xu, J., Nakae, J., Meseck, M., and Dong HH. Foxo1 mediates insulin action on apoC-III and triglyceride metabolism. J. Clin. Invest. 114:1493-1503. 2004. PMCID: PMC525736.
  2. Qu S., Altomonte J., Perdomo G., He J., Fan Y., Kamagate A., Meseck M. and Dong HH. Aberrant FoxO1 function is associated with impaired hepatic metabolism. Endocrinology. 147:5641-5652. 2006. PMCID: PMC2665253.
  3. Kamagate A., Qu S., Perdomo G., Kim DH., Slusher S. Meseck, M and Dong HH. FoxO1 mediates insulin-dependent regulation of hepatic VLDL production. J. Clin. Invest. 118:2347-2364. 2008. PMCID: PMC2391277.
  4. Su D, Coudriet GM, Kim DH, Lu Y, Perdomo G, Qu S, Slusher S, Tse HM, Piganelli J, Giannoukakis N, Zhang J, Dong HH. FoxO1 links insulin resistance to proinflammatory cytokine IL-1 production in macrophages. Diabetes. 58: 2624-33, 2009. PMCID: PMC2768186.
  5. Kamagate A, Kim DH, Zhang T, Slusher S, Gramignoli R, Strom SC, Bertera S, Ringquist S, Dong HH. Forkhead box O1 links hepatic insulin action to endoplasmic reticulum stress. Endocrinology. 2010 151:3521-3535. PMCID: PMC2940535.
  6. Kim DH, Perdomo G, Zhang T, Slusher S, Phillips BE, Fan Y, Giannoukakis N, Gramignoli R, Strom S, Ringquist S and Dong HH. FoxO6 integrates insulin signaling to gluconeogenesis in the liver. Diabetes. 60:2763-2774. 2011. PMCID: PMC3198083.
  7. Xiao G, Zhang T, Yu S, Lee S, Calabuig-Navarro V, Yamauchi J, Ringquist S, Dong HH. ATF4 deficiency protects against high fructose-induced hypertriglyceridemia in mice. J Biol Chem. 2013 288(35):25350-61. PMCID: PMC3757199.
  8. Kim DH, Zhang T, Lee S, Calabuig-Navarro V, Yamauchi J, Piccirillo A, Fan Y, Uppala R, Goetzman E, Dong HH. FoxO6 Integrates Insulin Signaling with MTP for Regulating VLDL Production in the Liver. Endocrinology. 155(4):1255-67. 2014. PMCID: PMC3959596.
  9. Zhang T, Kim DH, Xiao X, Lee S, Gong Z, Muzumdar R, Calabuig-Navarro V, Yamauchi J, Harashima H, Wang R, Bottino R, Carlos Alvarez-Perez J, Garcia-Ocaņa, Gittes G, Dong HH. FoxO1 Plays An Important Role in Regulating Beta-Cell Compensation for Insulin Resistance in Male Mice. Endocrinology. 157(3):1055-70. 2016. PMID: 26727107.
  10. Liu YZ, Cheng X, Zhang T, Lee S, Xiao X, Gittes G, Qu S, Jiang C-L and Dong HH. Hypertriglyceridemia in the absence of hyperglycemia and insulin resistance does not cause beta-cell dysfunction in ApoC3 transgenic mice. J Biol Chem. 2016. 291(28):14695-705. PMID: 27226540.