670 W. Baltimore Street HSF III, Room 4042 Baltimore, MD 21201
Education and Training
- Hubei Medical University at Xianning, Hubei, China, MD, Medicine, 1985
- The Third Military Medical University, Chongqing, China, MS, Pathology, 1988
- Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China, PhD, Molecular and pathological basis of atherosclerosis, 1995
- University of Alberta School of Medicine, Alberta, Canada Postdoc, Lipid metabolism, 1996-1998
- University of Texas Southwestern Medical Center, Dallas, Texas, Postdoc, Lipid metabolism, 1998-2000
My long-term goal is to identify the molecular mechanisms underlying lipid metabolism and transport and to define how these mechanisms influence the pathogenesis of common diseases, such as obesity, insulin resistance, diabetes, nonalcoholic fatty liver disease (NAFLD), and cardiovascular diseases. I have a broad background in biomedicine through clinical practice (Pathologist and Cardiologist) and basic research. I completed my postdoctoral training first in the lipid and lipoprotein group at the University of Alberta in Canada with Dr. Luis B. Agellon and later in the Department of Molecular Genetics at UT Southwestern Medical Center in Dallas with Dr. Helen H. Hobbs.
In 2004 I started my own lab at Wake Forest University School of Medicine, working on the role of NPC1L1 in cholesterol transport and metabolic disease, and recently on the role of intracellular lipid droplet lipolysis in the pathogenesis of metabolic disorders. I singlehandedly created several transgenic and knockout mouse models, and served as the Director of the Institutional Transgenic Mouse Core Facility at Wake Forest University School of Medicine for more than 7 years, demonstrating my strong background on molecular biology, genetics and genetic manipulations of mice.
In 2005, I started teaching students the advanced topics of Molecular and Cell Biology as well as Lipid Metabolism first at Wake Forest and later at University of Maryland, which ensures timely update of my knowledge in these areas. As a core faculty in the Georgia State University’s Center for Molecular and Translational Medicine, and now in the Division of Endocrinology, Diabetes and Nutrition at University of Maryland School of Medicine, I have close interactions with colleagues who share common research interests. These daily intellectual exchanges secure successful completion of our research projects.
lipid metabolism and transport, nafld, cardiovascular disease
See Pubmed for complete list of published work.
Awards and Affiliations
- Chinese Association of Cell Biology Award, 1988
- Ministry of Education of the People’s Republic of China Award, 1997
- David L. Williams Memorial Lectureship Award, 2006
- Aspen Lipid Conference, 2006
- Consultant, Merck & Co., 2006
Grants and Contracts
Ongoing Research Support
R01 (NIH/NIDDK) 07/18/2016—06/30/2020
Cellular and Molecular Mechanisms of Fatty Liver Disease
The major goal of this project is to identify the cellular and molecular bases for nonalcoholic fatty liver disease (NAFLD) progression using a novel mouse model that develops NASH and hepatic fibrosis on regular chow.
AHA (Grant-in-Aid) 07/01/2017—06/30/2019
Macrophage Triglyceride Hydrolysis and Atherosclerosis
The major goal of this project is to determine whether deficiency of lipid droplet lipolysis in macrophages influences atherogenesis in apoE knockout mice.
ADA 1-18-IBS-346 01/01/2018—12/31/2020
Brown fat lipolysis deficiency-induced thermoregulation and metabolic adaptation
The major goal of this project is to examine the effects of brown fat CGI-58 gene deficiency on thermogenesis and energy metabolism.
R01 (NIH/NIDDK) 06/15/2018 – 05/31/2022
The Role of Adipose Lipolysis in Thermoregulation
The major goal of this project is to molecularly define how adipose lipolysis regulates thermogenesis and metabolic health under different environmental and nutritional conditions.
R01 (NIH/NIDDK) 05/25/2018 – 04/30/2022
Epigenetic programming of beta-klotho in non-alcoholic fatty liver disease
The major goal of this project is to define how FGF21 resistance occurs and promotes fatty liver during chronic overnutrition.
R01 (NIH/NIDDK) 04/01/2019 – 03/30/2024
Coactivator regulates hepatic lipid metabolism and insulin signaling in obesity
The major goal of this project is to molecularly define how P300 coactivator regulates the pathogenesis of fatty liver and insulin resistance.
Role: Co-PI (Lead PI: Ling He at Johns Hopkins)
Completed Research Support
R01 (NIDDK) 04/01/2010-- 09/30/2016
NPC1L1 and Metabolic Diseases
The major goal of this project is to define how deficiency of a cholesterol transporter named NPC1L1 protects mice from high fat diet-induced obesity, glucose intolerance and insulin resistance.
Hisun Pharm (Industry) Grant 06/15/2013—06/14/2015
Hisun Pharm compound HS-25 and NPC1L1-dependent cholesterol absorption
The major goal of this project is to test whether HS-25 is an inhibitor of NPC1L1-depedent cholesterol absorption
Scientist Development Grant 07/01/2006 – 06/30/2010
American Heart Association
Ezetimibe modification of hepatic Niemann-Pick C1-Like 1 function
The major goal of this project is to determine whether ezetimibe inhibits hepatic NPC1L1
ZETIA/VYTORIN Investigator-Initiated Studies 011/01/2008-10/31/2010
The role of hepatic NPC1L1 and ezetimibe in reverse cholesterol transport
The major goal of this project is to determine whether hepatic NPC1L1 inhibits reverse cholesterol absorption
ZETIA/VYTORIN Investigator-Initiated Studies 08/01/2008-07/31/2010
Effects of intestinal overexpression of NPC1L1 on cholesterol metabolism
The major goal of this project is to genetically demonstrate a critical role of intestinal cholesterol absorption in production of atherogenic lipoprotein-cholesterol.
Pfizer Pharmaceuticals Atorvastatin Research Award 07/01/2005 – 06/30/2006
Role of the sterol-sensing domain in Niemann-Pick C1-Like 1 trafficking and function.
The major goal of this project it to define how the sterol-sensing domain (SSD) of NPC1L1 regulates NPC1L1’s subcellular localization in response to cells’ cholesterol availability.