Lily Q. Dong, Ph.D.Professor
Iowa State University, 1991
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. 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 (Mao et al., 2006, Nature Cell Biology, 8: 516-523) and in vivo (Ryu et al, 2014, Cell Reports, 1227-1238). 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 (Wang et al., 2009, JBC, 284, 31608-31615). Recently, we have demonstrated that APPL1 mediates the insulin sensitizer role of adiponectin by facilitating the binding of IRS1/2 to the insulin receptor in response to adiponectin stimulation (Ryu et al, 2014, Cell Reports, 1227-1238). The findings from our studies provide potential mechanisms behind insulin resistance and the development of type 2 diabetes.
She received the Graduate Teaching Award (Cellular & Structural Biology Department) in 2008 and Presidential Teaching Excellent Award (UTHSCSA) in 2013.
She is a Master Teacher named by the University of Texas Health Science Center and a Distinguished Teaching Professor awarded by the University of Texas Board of Regents.
Liu M, Bai J, He S, Villarreal R, Hu D, Zhang C, Yang X, Liang H, Slaga TJ, Yu Y, Zhou Z, Blenis J, Scherer PE, Dong LQ, Liu F. Grb10 promotes lipolysis and thermogenesis by phosphorylation-dependent feedback inhibition of mTORC1. Cell Metab. 2014 Jun 3;19(6):967-80.
Yu L, Tu Q, Han Q, Zhang L, Sui L, Zheng L, Meng S, Tang Y, Xuan D, Zhang J, Murray D, Shen Q, Cheng J, Kim SH, Dong LQ, Valverde P, Cao X, Chen J. Adiponectin regulates bone marrow mesenchymal stem cell niche through a unique signal transduction pathway - an approach for treating bone disease in diabetes. Stem Cells. 2014 Sep 3.
Wu Y, Tu Q, Valverde P, Zhang J, Murray D, Dong LQ, Cheng J, Jiang H, Rios M, Morgan E, Tang Z, Chen J. Central adiponectin administration reveals new regulatory mechanisms of bone metabolism in mice. Am J Physiol Endocrinol Metab. 2014 Jun 15;306(12):E1418-30.
Ou X, Liu M, Luo H, Dong LQ, Liu F. Ursolic acid inhibits leucine-stimulated mTORC1 signaling by suppressing mTOR localization to lysosome. PLoS One. 2014 Apr 16;9(4):e95393.
Mao X, Kikani CK, Riojas RA, Langlais P, Wang L, Ramos FJ, Fang Q, Christ-Roberts CY, Hong JY, Kim RY, Liu F, Dong LQ. APPL1 binds to adiponectin receptors and mediates adiponectin signalling and function. Nat Cell Biol. 2006 May;8(5):516-23.
Lim MA, Kikani CK, Wick MJ, Dong LQ. Nuclear translocation of 3'-phosphoinositide-dependent protein kinase 1 (PDK-1): a potential regulatory mechanism for PDK-1 function. Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14006-11.