Lily Q. Dong, Ph.D.Professor
Iowa State University, 1991
Dr. Dong is a Professor of Cellular & Structural Biology at the University of Texas Health Science Center at San Antonio. She received Ph.D. from Iowa State University and did post-doctoral training at Stanford University. Dr. Dong's research is focused on obesity and type 2 diabetes. She is interesting in how adiponectin acts as an insulin sensitizer to regulating energy homeostasis, and glucose and lipid metabolism. Dr. Dong has been an active member of the American Diabetes Society. She was a recipient of Career Development Award (2004-2009) from American Diabetes Association and is currently serving on ADA Research Grant Review Committee. Dr. Dong also participates in graduate student teaching and received the Departmental Graduate Teaching Award (2008). She was named as an Academic Member by the University of Texas Health Science Center and awarded as a Distinguished Teaching Professor by the University of Texas Board of Regents in 2010.
Insulin resistance is a primary contributing factor in the pathogenesis of type 2 diabetes. This condition is characterized by the loss of insulin sensitivity in insulin target tissues, resulting in an impairment of glucose breakdown and an unregulated production of glucose in hepatic cells, and a reduction of glucose uptake in skeletal muscle, which causes a greatly increased glucose level in the bloodstream. Adiponectin is a hormone secreted from adipose tissue. The serum concentration of adiponectin is significantly reduced in type 2 diabetic and obese patients. A number of studies have shown that adiponectin is an insulin sensitizer by enhancing insulin sensitivity, suggesting that the molecules in adiponectin signal pathways could be targets of therapeutic drug development for the treatment of type 2 diabetes and obesity. However, the molecular mechanism governing adiponectin action is largely unknown.
Our research interest is mainly focused on: 1) the elucidation of the molecular pathway(s) mediating adiponectin signaling in cells and in vivo; and 2) the investigation of the molecular mechanism of the cross-talk between insulin signaling pathway and adiponectin signaling pathway.
We have identified APPL1, an adaptor protein with multiple function domains, as the first signaling molecule immediate binding to adiponectin receptors, and positively mediating adiponectin signaling in muscle cells (Figure 1) (Mao et al., 2006, Nature Cell Biology, 8: 516-523, PMID: 16622416). Our work has been described by peers as "identifying a novel mechanism linking adiponectin to insulin sensitization" and "opening doors to exciting avenues of investigation in adiponectin signaling system" (Research Highlight Commentary by Hosch et al, 2006, in Cell Metabolism, 4, 5-6). This publication was the highlighted research article on the cover page of the issue of Nature Cell Biology.
In addition, we have shown that APPL2, an isoform of APPL1, negatively regulates adiponectin signaling. We proposed that APPL1/APPL2 isoforms function as an integrated "Yin-Yang" regulator in adiponectin signaling (Figure 2) (Wang et al., 2009, JBC, 284, 31608-31615, PMID:19661063). The findings from our studies provide potential mechanisms behind insulin resistance and the development of type 2 diabetes.
General techniques in signal transduction
Yeast two-hybrid system
Confocal optical imaging
Lipid and glucose assays
Genetic mouse model generation
(Publications before 1997 were under the name of Dong, Q.)
Ryu, J., Galan, A.K., Xin, X., Dong, F., Abdul-Ghani, M.A., Zhou, L., Wang, C., Li, C., Holmes, B.M., Sloane, L.B., Austad, S.N., Guo, S., Musi, N., DeFronzo, R.A., Deng, C., White, M.F., Liu, F., Dong, L.Q. (2014)
APPL1 Potentiates Insulin Sensitivity by Facilitating the Binding of IRS1/2 to the Insulin Receptor.
Cell Rep. 2014 May 7. pii: S2211-1247(14)00293-9.
Wu, Y., Tu, Q., Valverde, P., Zhang, J., Murray, D., Dong, L.Q., Cheng, J., Rios, M., Morgan, E., Tang, Z., Chen, K. (2014)
Central Adiponectin Administration Reveals New Regulatory Mechanisms of Bone Metabolism in Mice.
Am J Physiol Endocrinol Metab. 2014 Apr 29.
Liu, M., Bai, J., He, S., Villarreal, R., Hu, D., Zhang, C., Yang, X., Liang, H., Slaga, T., Yu, Y., Zhou, Z., Blenis, J., Scherer, P.E., Dong, L.Q., Liu, F. (2014) Grb10 Promotes Lipolysis and Thermogenesis by Phosphorylation-dependent Feedback Inhibition of mTORC1. Cell Metab. 2014 Apr 15. pii: S1550-4131(14)00123-5.
Qu, X., Liu, M., Luo, H., Dong, L.Q., Liu, F. (2014) Ursolic Acid Inhibits Leucine-Stimulated mTORC1 Signaling by Suppressing mTOR Localization to Lysosome. PLoS One. 2014 Apr 16; 9(4):e95393.
Mao, X., Kikani, C. K., Riojas, R. A., Langlais, P., Wang, L., Ramos, F. J., Fang, Q., Christ-Roberts, C.Y., Hong, J.Y., Kim, R. Y., Liu, F., Dong, L. Q. (2006) APPL1 bonds to adiponectin receptors and mediates adiponectin signaling and function. Nat Cell Biol. 2006 May; 8(5):516-23.