Regulation of immunometabolism in adipose tissue

Abstract

Adipose tissue has emerged as a major player in driving obesity-related inflammatory response. In obesity, chronic infiltration of macrophages in adipose tissue mediates local and systemic inflammation and acts as a key contributor to insulin resistance. In the past few years, adipose tissue plasticity and remodeling capacity has been studied extensively to develop therapeutic targets to combat obesity and related metabolic dysfunction. Progress in understanding the potential of adipocytes and contribution of macrophages and other immune cells to control immunometabolism in disease state has provided us new potential intervention targets to explore such as the formation of heat-producing beige adipocytes in white adipose tissue and the polarization of macrophages from an inflammatory toward an anti-inflammatory phenotype. Initiation and progression of inflammatory signaling in fat pads is complex, broad, and often functions in a tissue/cell type-specific manner. We have also realized the importance of location, coordinated role of tissue cross-talk, and physiological state of the fat pad in these processes. There has been significant progress in understanding how adipose tissue regulates these crucial processes and maintains metabolic homeostasis such as identification of fat depot-specific regulation of energy metabolism, mediators of macrophage polarization, role of gut-derived antigens, and consequences of diet and calorie restriction on adipose tissue metabolic and thermogenic potential.

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