Abstract
Adipose tissue macrophages (ATM) are a major source of low-grade inflammation in obesity, and yet reasons driving ATM accumulation in white adipose tissue (WAT) are not fully understood. Emerging evidence suggested that ATM underwent extensive remodeling in obesity. In addition to abundance, ATM in obesity were lipid-laden and metabolically reprogrammed, which in turn was tightly related to their functional alterations and persistence in obesity. Herein, we aimed to discuss that activation of lipid sensing signaling associated with metabolic reprogramming in ATM was indispensible for their migration, retention, or proliferation in obesity. Likewise, lipolysis also induced similar but transient ATM remodeling. Therefore, we assumed that obesity might share overlapping mechanisms with lipolysis in remodeling ATM. Formation of crown-like structures (CLS) in WAT was presumably a common event initiating ATM remodeling, with a spectrum of lipid metabolites released from adipocytes being potential signaling molecules. Moreover, adipose interlerkin-6 (IL-6) exhibited homologous alterations by obesity and lipolysis. Thus, we postulated a positive feedback loop between ATM and adipocytes via IL-6 signaling backing ATM persistence by comparison of ATM remodeling under obesity and lipolysis. An elucidation of ATM persistence could help to provide novel therapeutic targets for obesity-associated inflammation.
Highlights
The prevalence of Western dietary pattern and sedentary lifestyle boosted the pandemic of obesity worldwide, which was closely associated with increased risks of various metabolic disorders [1]
In this review, supported with current literature, we proposed the existence of a positive feedback loop between adipocytes and adipose tissue macrophages (ATM) via IL-6 signaling in obesity and white adipose tissue (WAT) lipolysis concerning ATM persistence, in hoping to provide new insights for studies of obesity-related inflammation
Metabolic reprogramming associated with activation of lipid sensing signaling in ATM might be an important mechanism for ATM accumulation in obesity
Summary
The prevalence of Western dietary pattern and sedentary lifestyle boosted the pandemic of obesity worldwide, which was closely associated with increased risks of various metabolic disorders [1]. ATM in obese mice and humans overexpressed various cell surface receptors to uptake lipids derived from adipocytes in CLS, many of which were indispensable for ATM accumulation in obesity [13, 14]. In this regard, it was postulated that adipocytes could crosstalk with ATM via secretion of diverse lipid metabolites and activated lipid sensing signaling in ATM, which could be another key mechanism underlining obesity-linked ATM accumulation. In this review, supported with current literature, we proposed the existence of a positive feedback loop between adipocytes and ATM via IL-6 signaling in obesity and WAT lipolysis concerning ATM persistence, in hoping to provide new insights for studies of obesity-related inflammation
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