Adipose (fat) tissue is an important organ for energy storage, insulation, and hormone regulation; however, larger quantities of body fat are linked with the development of cardiovascular diseases and diabetes. While weight loss is often prescribed to reduce disease risk, weight loss is difficult to do and even more difficult to maintain. Importantly, weight regain is linked to a heightened risk for cardiometabolic diseases beyond the risk of obesity itself.

Nearly all immune cells are found in the adipose tissue. Regulatory and “anti-inflammatory” immune cells reside in lean fat, while adipose expansion recruits and alters immune cells to become more “inflammatory” [1,2]. Interestingly, many of the drugs used in the clinic for high cholesterol and diabetes also have anti-inflammatory effects. Thus, we believe that adipose immune cells can be a useful therapeutic target for many metabolic diseases.

In my postdoctoral studies, I found that weight loss can induce a “memory” to the state of obesity in adipose macrophages in mice [3,4]. Although weight loss does improve diabetes risk, macrophages in the adipose tissue remain hypermetabolic (with higher glycolysis and oxidative phosphorylation) and hyperinflammatory (with greater secretion of inflammatory cytokines). We believe this heighted inflammation mediates the worsened diabetes risk upon weight regain. Additionally, my postdoctoral work found that weight regain induces a novel lipid handling phenotype in adipose mast cells [3 and manuscript in review].

The goal of my research group is to uncover the mechanisms that drive macrophage memory and mast cell lipid handling and how these cells may contribute to diabetes and sepsis with weight gain, weight loss, and weight cycling. Moreover, we will assess how exercise and different nutritional and therapeutic strategies may affect weight cycling and inflammation.