We study how obesity impacts health. The growing worldwide obesity epidemic is frequently linked to hyperlipidemia, inflammation, and insulin resistance leading to increased risk of diabetes, cardiovascular disease, and several kinds of cancer. The long-term goal of our laboratory is to determine mechanisms by which obesity increases risk for and pathophysiological consequences of these devastating diseases. Macrophages are part of the innate immune system that infiltrate white adipose tissue (fat) in obese rodents and humans, and produce most of the inflammatory cytokines and chemokines secreted from adipose tissue. In addition, their presence has been shown to be temporally associated with the development of insulin resistance. Our current research focus is threefold: to determine mechanisms by which macrophages accumulate in adipose tissue, to determine the role of resident macrophages in normal adipose tissue function, and to determine how other immune cells like eosinophils and T cells also contribute to adipose tissue function.

Macrophage Iron Metabolism:
Not much is known about the role of adipose tissue macrophages in tissue homeostasis. Our recent data suggests that resident M2-like macrophages may play a role in iron metabolism in fat. These exciting findings have opened up a new area of research for our group to assess the impact of macrophage iron handling on adipose tissue homeostasis.

Weight Loss and Weight Cycling:
A growing number of human studies have identified that body weight variability is a risk factor for progression of metabolic disease. We have generated a novel mouse model of weight cycling and observed that a subset of CD8+ Memory T cells is highly elevated in adipose tissue of weight cycled mice compared to obese controls. We have ongoing studies to elucidate the trafficking, clonality, and inflammatory profile of these memory T cells during obesity, weight loss, and weight cycling.