Weiqin Chen, PhD

 Professor

Phone: (706) 721-8706  
Fax: (706) 721-7299 
Email: wechen@augusta.edu
Office: CA-3094
Lab: CA-3093

 

 

 

 

Professional Experience

2005-2010      Postdoctoral Associate, Endocrinology & Metabolism with Dr. Lawrence Chan, Department of Medicine,
                         Baylor College of Medicine, Houston TX.

2010-2012       Instructor, Endocrinology & Metabolism, Diabetes & Endocrinology Research Center (DERC),
                          Baylor College of Medicine, Houston TX.

2012-2018        Assistant Professor, Department of Physiology, Augusta University, Augusta GA.

2018-present   Associate Professor, Department of Physiology, Augusta University, Augusta GA.

Research Interests

The research in my laboratory is directed toward understanding mechanisms that regulate nutrient and energy metabolism, and how they become reprogrammed in obesity, lipodystrophy, and cardiometabolic diseases. We are specifically interested in the following areas: (1) Adipose biology and energy balance in obesity and lipodystrophy; (2) Cardiac substrate utilization in heart failure; (3) Lipid metabolism in liver pathophysiology. Using in vitro molecular/cellular biology approaches, a combination of genomics, transcriptomics, proteomics, CRISP/Cas9-mediated genome editing, and state-of-the-art in vivo mouse physiology analyses, we aim to define the pathological alterations of metabolic communication in diseases including obesity, diabetes, and their associated liver and heart diseases. Ultimately, we aim to identify targets and design therapeutics for these diseases.

Current Projects

To understand the mechanisms underlying adipose tissue development in obesity and lipodystrophy.

Obesity and its associated health comorbidities are a worldwide epidemic with serious economic and health burdens on society. Adipose tissue is a vital endocrine organ that plays a crucial role in developing obesity and various metabolic disorders. White adipocytes store excess energy in the form of triglycerides for future needs. By contrast, brown and beige (browning-in-white) adipocytes metabolize lipids and glucose to produce heat in a process known as nonshivering thermogenesis, which is crucial in systemic energy homeostasis and thermoregulation. Functional brown and beige adipose tissues are highly correlated with body mass index in adult humans and are either reduced or absent in obese and aged individuals and rodents. We are among the first to create the lipodystrophic Bscl2 global knockout mice and reveal the novel role of BSCL2 in regulating white and brown adipocyte differentiation, maintenance, and function, thus lipodystrophy and its associated comorbidities. We are now uncovering the molecular functions of posttranslational modifications (neddylation) and important GWAS-identified genes in adipose tissue development, obesity and lipodystrophy.

 

 

To investigate how altered lipid metabolism contributes to metabolic cardiomyopathy.

Metabolic perturbations underpin a wide variety of cardiomyopathies. In healthy humans, oxidation of FA is the dominant energy source for myocardial function and accounts for 60-70% of oxygen consumption. In obesity and diabetes, elevated FA supply chronically raises FA oxidation (FAO) in the heart, reducing cardiac efficiency and developing cardiac lipotoxicity. Heart TGs not only supply cardiomyocytes with FAs but are critical for the regulation of heart function. We have demonstrated the essential role of BSCL2 in regulating cardiac substrate utilization and function. We seek to advance our understanding of the novel players and mechanisms underlying cardiac TG lipolysis, mitochondrial function, and metabolic cardiomyopathy.

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To probe the links between lipid metabolism and liver pathophysiology in obesity and diabetes.

Nonalcoholic fatty liver disease (NAFLD), which ranges from NAFL to nonalcoholic steatohepatitis (NASH) and cirrhosis, is an underdiagnosed complication of obesity and type 2 diabetes (T2D). Up to 70% of patients with T2D have NAFLD, and people with diabetes have much higher rates of NASH, cirrhosis, and hepatocellular carcinoma (HCC) than the general, non-diabetic population. Hepatocellular death is a cardinal feature of NASH, which causes inflammation, fibrosis, cirrhosis and HCC. Therapeutic options for NAFLD in obesity and T2D are currently limited. A critical barrier to treatment is the lack of understanding of the molecular mechanisms that control hepatocellular death in NAFLD and NASH. We have demonstrated an essential role of NAE1-mediated neddylation in regulating liver development and function. We are interested in identifying novel player(s) that directly control lipotoxicity-induced hepatocellular death and facilitate the irreversible progression of NAFL to NASH in obesity and T2D.

 

Awards and honors 

2017 Outstanding Young Basic Science Faculty Award from MCG Faculty Senate

2013 RNA-Seq Grant, Augusta University Cancer Center

2013 Eugenia Rosenberg Travel Award, Endocrine Society

2008 Postdoctoral Fellowship, American Heart Associatio

2006 Mentor Based Postdoctoral Fellowship, American Diabetes Association

2004 DuVall Award (Excellent graduate student scholarship), Michigan State University