Dysregulation of Fat Tissue and Immune Response in Obesity
  • Jae Bum Kim Ph.D
  • SLS Colloquia / April 26th 04:00 pm / BLDG 110 / ROOM N104
Abstract

Adipose tissue plays key roles in whole body energy homeostasis. Accumulating evidence has suggested that obesity is characterized by chronic and low-grade inflammation accompanied by macrophage accumulation in the adipose tissue, which eventually leads to metabolic diseases, including insulin resistance and type 2 diabetes. The increased number of adipose tissue macrophages (ATMs) plays crucial roles in the altered production of proinflammatory cytokines in the fat tissue of obese individuals. In healthy lean mice, ATMs are mostly composed of alternatively activated (M2) type macrophages that express high levels of anti-inflammatory cytokines, such as IL-10, and specific enzymes, such as arginase 1 (ARG1), in addition to low levels of proinflammatory signals. It is likely that M2 ATMs contribute to metabolic homoeostasis by preventing adipose tissue inflammation. However, in the progression of obesity, some ATMs are polarized into the classically activated (M1) type. In the adipose tissue of obese individuals, M1 ATMs stimulate iNOS and the secretion of proinflammatory cytokines such as TNFa, IL-6, and IL-1b. Thus, the imbalance between M1- and M2-like ATMs appears to be crucial to stimulating pro-inflammatory responses in obese adipose tissue. In this presentation, I will discuss that alteration of lipid metabolism in ATMs would be crucial to induce inflammatory responses and insulin resistance in obesity.