Cancer Prevention Program
A hallmark of obesity is excess lipid accumulation in adipocytes in subcutaneous and visceral adipose tissue depots. This increase in adiposity is associated with low-grade chronic adipose tissue inflammation, which is thought to be a key mediator between obesity, insulin resistance, and glucose intolerance leading to type 2 diabetes. Macrophages play a key role in adipose tissue inflammation. The objective of this study is to understand the mechanisms that produce the pro-inflammatory activation of adipose tissue macrophages (ATMs), and to understand how ATMs contribute to insulin resistance in obese patients. We will recruit 75 individuals over five years falling into three groups (25 per group): 1) non-obese and insulin sensitive, 2) obese and insulin sensitive, and 3) obese and insulin resistant. This approach will allow us to dissociate the relationship between adiposity, adipose tissue inflammation, and insulin resistance. Participants will be recruited from an outpatient surgery center. Subcutaneous and visceral adipose tissue samples will be collected from participants during surgery for analysis of adipose tissue inflammation and the characterization and isolation of ATMs. Participants will also be admitted to clinic for assessment of glucose tolerance, insulin sensitivity, and pancreatic beta-cell function by oral glucose tolerance test, assessment of liver fat by magnetic resonance imaging scan, and assessment of body composition by dual-energy x-ray absorptiometry scan.