Ke Ma, M.D., Ph.D.
Education and Training
M.D. Shandong Medical University, Shandong, China
Endocrinology, Diabetes, and Metabolism Fellowship, Baylor College of Medicine, Houston, Texas
Dr. Ma received her M.D. degree from the Shandong Medical University in Shandong, China in 1994, and her Ph.D. from the Baylor College of Medicine in Houston, Texas in 2003. She then completed two postdoctoral fellowships at Baylor, the most recent one under the mentorship of Dr. David D. Moore in the Department of Molecular and Cellular Biology. With Dr. Moore and others, Dr. Ma has published papers in some of the most prestigious medical journals, including a first-author paper in the Proceedings of the National Academy of Sciences. While at Baylor, she received an American Heart Association Postdoctoral Fellowship Award. Dr. Ma joined The Methodist Hospital Research Institute in 2010.
Dr. Ma conducts translational research that studies the connection between circadian disruption and metabolic dysfunction as seen in diabetes and cardiovascular disease. Her previous research demonstrated that hepatic bile acid homeostasis is under the coordinated control of the central and peripheral clock and disruption through restricted feeding or genetic ablation (silencing of Per1-/-/Per2-/-) leads to cholestasis and liver injury. Her current studies focus on identifying the effect of circadian regulation on glucose and lipid homeostasis and how the disruption through genetic and pharmacological approaches would lead to the development of diabetes and other related metabolic diseases. The long-term goal of this research is to identify specific metabolic pathways affected by circadian clock and uncover new regulatory pathways that lend themselves to interventions using selective ligands that modulate activity of the nuclear receptors involved in these processes.
Circadian rhythm, metabolism, diabetes, cardiovascular disease, genomic medicine.
Ma K, Xiao R, Tseng HT, Shan L, Fu L, Moore DD. Circadian dysregulation disrupts bile acid homeostasis. PLoS One. 2009 Aug 31;4(8):e6843.
Huang W, Ma K, Zhang J, Qatanani M, Cuvillier J, Liu J, Dong B, Huang X, Moore DD. Nuclear receptor-dependent bile acid signaling is required for normal liver regeneration. Science. 2006 Apr 14;312(5771):233-6.
Ma K, Saha PK, Chan L, Moore DD. Farnesoid X receptor is essential for normal glucose homeostasis. J Clin Invest. 2006 Apr;116(4):1102-9.
Ko KW, Paul A, Ma K, Li L, Chan L. Endothelial lipase modulates HDL but has no effect on atherosclerosis development in apoE-/- and LDLR-/- mice. J Lipid Res. 2005 Dec;46(12):2586-94.
Ma K, Forte T, Otvos JD, Chan L. Differential additive effects of endothelial lipase and scavenger receptor-class B type I on high-density lipoprotein metabolism in knockout mouse models. Arterioscler Thromb Vasc Biol. 2005 Jan;25(1):149-54.
Ma K, Cilingiroglu M, Otvos JD, Ballantyne CM, Marian AJ, Chan L. Endothelial lipase is a major genetic determinant for high-density lipoprotein concentration, structure, and metabolism. Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2748-53.