Adipose tissue's rapid response team

Abstract

Adipose tissues function in metabolic, endocrine, and immune roles to regulate energy balance and maintain health. Adipocytes reside within adipose tissues (so-called depots) together with fibroblasts, adipose progenitors, endothelial cells, and immune cells. Collaboration among these multiple cell types is necessary for the tissue to remodel and maintain homeostasis in the face of metabolic challenges. 1 In nonobese individuals, resident adipose tissue macrophages (ATMs) are mainly M2-like and function to remodel the tissue as needed for growth, maintenance, and repair. With chronic overnutrition and obesity, adipocytes expand in size to accommodate the need for energy storage and become dysfunctional. As a result, monocytes are recruited into adipose tissue in a CCL2 (MCP-1)-dependent manner. These ATMs localize around dead or dying adipocytes in the so-called crown-like structures, where they become M1 polarized and increase production of inflammatory cytokines. 2 The result is a feed-forward cycle within the adipose tissue, which is thought to lead to adipocyte metabolic and endocrine dysfunction, most notably excessively high release of potentially lipotoxic fatty acids and lower production of the antiinflammatory hormone adiponectin. The resulting adipocyte and systemic insulin resistance and dyslipidemia mechanistically links obesity to disease risk.Virtually all studies that led the macrophage recruitment hypothesis used obesity-prone male C57BL/6 mice fed a very high fat diet (HFD; usually 60% fat calories) for a prolonged period, at least 3 months, to induce obesity. However, analysis of the established obese state cannot reflect the dynamics of its development and hence its etiology, as Muir et al. 3 have accomplished in this issue ofThe author declares no conflict of interest