H. Henry Dong, PhD
Professor of Pediatrics


Dr. Dong is a member of the Cellular and Molecular Pathology Graduate Training Program. Dr. Dong currently serves as Associate Vice Chair for Research in Department of Pediatrics. Dr. Dong is a member of the Pittsburgh Liver Research Center.

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
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

Mechanism of beta-cell compensation in gestational diabetes and type 2 diabetes: 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 compensation, known as an adaptive mechanism by which pancreatic beta-cells increase insulin secretion to overcome insulin resistance for maintaining normal blood sugar levels in individuals with overweight or obesity. Beta-cell compensation culminates in the expansion of beta-cell mass and upregulation of insulin synthesis and secretion. Failure of beta-cells to compensate for insulin resistance contributes to insulin insufficiency and type 2 diabetes. Likewise, beta-cell compensation ensues in women during pregnancy. Pregnancy is associated with maternal insulin resistance in the 3rd trimester during pregnancy, a physiological response that serves to spare blood glucose supplies for the fetus. Inept beta-cell compensation for maternal insulin resistance is an underlying cause of gestational diabetes. To date, how beta-cells compensate for insulin resistance and what causes beta-cell failure in gestational diabetes and type 2 diabetes are poorly understood. Dr. Dong's team works to characterize genetic factors that integrate insulin resistance to beta-cell compensation for obesity and pregnancy in animal models with morbid obesity or gestational diabetes. Such genetic factors could be potential therapeutic targets for augmenting beta-cell compensation to prevent the development of overt diabetes in at-risk individuals with gestational diabetes and type 2 diabetes.

Pathophysiology of insulin resistance and diabetic dyslipidemia:

A second focus of Dr. Dong's laboratory is on diabetic dyslipidemia, the most common lipid disorder in patients with obesity and type 2 diabetes. Diabetic dyslipidemia is characterized by a triad plasma lipid profile, i.e., increased triglyceride and LDL-cholesterol levels, and decreased HDL-cholesterol levels. Diabetic dyslipidemia is considered an independent risk factor for coronary artery disease. Using transgenic, gene knockout and gene transfer approaches, Dr. Dong's team works to characterize the insulin-Akt-FoxO signaling pathway in glucose and lipid metabolism in the liver and extrahepatic tissues. These studies are expected to gain insight into the molecular events that link insulin resistance to metabolic abnormalities, providing a knowledge base for the development of small molecule drugs for better clinical management of diabetic dyslipidemia in patients with morbid obesity and type 2 diabetes. Dr. Dong has received funds from National Institute of Health, American Diabetes Association and Juvenile Diabetes Research Foundation.

Selected Publications

View Dr. Dong's publications on PubMed

  1. Feng X, Zhu C, Lee S, Zhu P, Yamauchi J, Pan C, Singh, S, Qu S, Miller R, Monga SP, Peng Y, HH Dong. Depletion of hepatic forkhead box O1 does not affect cholelithiasis in male and female mice. J Biol Chem. 2020 April 9. [Epub ahead of print]. PMID:32273343.
  2. Xiao X, Chen C, Guo P, Zhang T, Fischbach S, Fusco JC, Shiota C, Prasadan K, Dong HH, Gittes GK. FoxO1 inhibits accelerated ?-cell aging in pancreas-specific SMAD7 mutant mice. J Biol Chem. 2017 292:3456-3465. PMID: 28057752.
  3. Cheng X, Yamauchi J, Lee S, Zhang T, Gong Z, Muzumdar R, Qu S, Dong HH. APOC3 Protein Is Not a Predisposing Factor for Fat-induced Nonalcoholic Fatty Liver Disease in Mice. J Biol Chem. 2017 292:3692-3705.
  4. Lee S, Dong HH. FoxO integration of insulin signaling with glucose and lipid metabolism. J Endocrinolology 2017 233:R67-R79. PMID:28213398.
  5. Xiao X, Fischbach S, Zhang T, Chen C, Sheng Q, Zimmerman R, Patnaik S, Fusco J, Ming Y, Guo P, Shiota C, Prasadan K, Gangopadhyay N, Husain SZ, Dong H, Gittes GK. SMAD3/Stat3 Signaling Mediates ?-Cell Epithelial-Mesenchymal Transition in Chronic Pancreatitis-Related Diabetes. Diabetes. 2017 66:2646-2658. PMID: 28775125.
  6. 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. 2016 157:1055-70. PMID: 26727107.
  7. 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. 291:14695-705. PMID: 27226540.
  8. Calabuig-Navarro V., Yamauchi J, Lee S, Zhang T, Liu YZ, Sadlek K, Goudriet GM, Piganelli JD, Jiang CL, Miller R, Lowe M, Harashima H, Dong HH. FoxO6 Depletion Attenuates Hepatic Gluconeogenesis and Protects Against Fat-Induced Glucose Disorder in Mice. J Biol Chem. 2015 290:15581-15594. PMID: 25944898.
  9. 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. 2014 155:1255-1267. PMID: 24437489.
  10. 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 288:25350-25361. PMID: 23888053