Henjiang (Henry) Dong, PhD

  • Professor of Pediatrics

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.

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. A second focus of 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, 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.

Dong has received funds from National Institute of Health, American Diabetes Association and Juvenile Diabetes Research Foundation.  

Professional and Scientific Society Memberships

  • American Diabetes Association, 1999-Present 
  • American Heart Association, 2007-2012 
  • New York Academy of Sciences, 2003-2012  
  • American Society of Gene Therapy, 2000-2003 

Education & Training

  • BS, Biochemistry, Henan Normal University, 1986
  • MS, Genetics, Chinese Academy of Science, 1989
  • PhD, Molecular Biology, Uppsala University, 1995
  • Postdoctoral Research in Cell Biology, Yale University, 1998

Selected Publications

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.  

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-Ocaña, 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.

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-1bproduction in macrophages. Diabetes. 58: 2624-33, 2009. PMCID: PMC2768186.

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.

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.

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.

Full Publication List via NIH PubMed »

Academic and Research Interests

NIH R01120310-0, DK Myeloid Fox O1 in A1 Lipid Metabolism, (PI, 25% effort), 2019-2023 

4100077074, Development of anti-fox O1 small molecule, (PI, 10% effort), 2017-2020, No-Cost Extension