Zhen Y. Jiang, M.D., Ph.D.

1-16-IBS-146-JiangAssociate Professor of Pharmacology and Medicine, Section of Endocrinology, Diabetes, Nutrition, and Member, The Whitaker Cardiovascular Institute
Department of Pharmacology

Ph.D. (Biochemistry): University College, University of London, London, U.K. M.D.: Jiangxi Medical College, Nanchang, Jiangxi, China. M.Sc. (Pharmacology): Institute of Materia Medica, Chinese Academy of Medical Science & Peking Union Medical College, Beijing, China.

Laboratory: Laboratory of Diabetes and Obesity Research

Research Interests

Metabolic Syndrome, Obesity, Diabetes and Innate Immunity
Currently, my lab mainly focuses on understanding how insulin signaling networks and innate immunity regulate metabolic functions.

1. CDP138 and its signal networks related to glucose and lipid metabolisms. In collaboration with Dr. Marcus Krueger and Dr. Matthias Mann’s laboratory at the Planck Institute of Biochemistry in Munich, Germany, we applied a SILAC-based quantitative proteomics approach and identified multiple phosphoproteins from insulin-stimulated adipocytes. As a result, we found that CDP138, a novel phosphoprotein containing C2 domain, is involved in the regulation of GLUT4 translocation. We also produced CDP138 knockout mouse model. Currently, we are using TIRF microscopy-based live cell imaging, protein-protein interactions, gene expression profiling and the knockout mouse model to study the signal network of CDP138 and its role in the regulation of glucose and lipid metabolisms and neuronal functions.

2. Exploring the role of neutrophils and neutrophil elastase (NE) in the development of obesity-related adipose inflammation, insulin resistance and cardiovascular dysfunction. Using quantitative serum proteomic approach, we recently identified that there is an imbalance between NE and its inhibitor alpha-1-antitrypsin in both obese human subjects and mouse models. Interestingly, both NE knockout mice and human A1AT transgenic mice are resistant to high-fat diet-induced body weight gain, adipose inflammation, fatty liver and insulin resistance. We also observed that NE knockout mice have higher AMP kinase activity and fatty acid oxidation rate. Currently, we are exploring molecular and cellular mechanisms whereby obesity regulates neutrophils activity and subsequent adipose inflammation, fatty liver, insulin resistance and cardiovascular dysfunctions using approaches such as live animal imaging, bone marrow transplantation, transcriptional regulation and lipidomics with different mouse models.