Lin Zhu, M.D., Ph.D.

Research Assistant Professor of Medicine

Division of Diabetes, Endocrinology, & Metabolism

Stafford Lab


Office Address:
2213 Garland Avenue, Medical Research Building, Room / Suite 7465, Nashville, TN 37232-0475
Diabetes, Endocrinology, & Metabolism

Dr. Zhu’s research interest is to understand the relationship between energy homeostasis and inflammation, which might be a foundational mechanism for insulin resistance, hyperlipidemia, and atherosclerosis. Her research focuses on the use of mouse disease models to identify mechanisms that underlie insulin resistance and atherosclerosis. She aims to define fundamental principles of how to improve HDL function for patients with type-2 diabetes to reduce cardiovascular disease. During Dr. Zhu’s graduate studies, she studied the regulation of PCYT2, a rate-limiting enzyme for phospholipid synthesis, at transcriptional and posttranscriptional levels. This work resulted in seven publications with four of them as the first author. During her training as a postdoctoral fellow in the Division of Cardiovascular Medicine at Vanderbilt, Dr. Zhu demonstrated that LRP1-deficient macrophages caused inflammatory responses in the artery walls due to the impaired ability of foam cells to clear the plaque. In another high-impact project, she found that anti-inflammatory macrophages promoted cholesterol reverse transport and macrophage migration out of artery walls, leading to atherosclerosis regression. This novel discovery may set up a platform to develop therapeutic policies to prevent cardiovascular events. During her training in the Division of Diabetes, Endocrinology, and Metabolism at Vanderbilt, Dr. Zhu showed that deletion of liver estrogen receptor alpha led to lipid accumulation in the liver and caused whole body insulin resistance. One of her ongoing projects shows that a clinically used CETP inhibitor increases HDL cholesterol; however, it also increases inflammatory responses and causes insulin resistance in obese mice. This study may explain the reason why clinical trials using CETP inhibitors have failed to prevent cardiovascular disease.