Qi Research Lab

The Metabolic Syndrome, obesity, and type 2 diabetes are reaching epidemic proportions and pose a significant medical and financial burden to the Western societies.   It is our long-term goal to elucidate the molecular mechanisms underlying the pathogenesis of insulin resistance in the hope that we might develop new therapies to prevent or combat obesity and type 2 diabetes.

Cross-sections and H&E staining of adipose tissue from obese mice.  Note: tissue section on the left panel exhibits massive lymphocytes infiltration indicated by arrows (such as macrophages).


Obesity is often associated with infiltration of macrophages into adipose tissues, which is thought to contribute significantly to insulin resistance. Despite considerable attention, however, there is little information so far on the mechanism by which adipocytes, through secretion of adipokines, regulate infiltrating macrophages to influence local and systemic inflammation. Our goal is to study the molecular basis of communication between macrophages and adipocytes in adipose tissues.  To this end, we use gene knockout and knockdown approaches to investigate the genetic control of inflammation in infiltrating macrophages and adipocytes.

Recent data suggest that endoplasmic reticulum (ER) stress response, partially caused by accumulation of malfolded proteins and ER overload, may play a key role in the development of insulin resistance and diabetes. However, the molecular mechanism underlying the hypothesis remains unknown. We are interested in the physiological role of ER stress in adipocytes and hepatocytes in the context of obesity and insulin resistance. Our laboratory intends to elucidate the regulation of ER stress responses using biochemical, genetic, immunological and high-throughput approaches.