M2-like macrophages serve as a niche for adipocyte progenitors in adipose tissue.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Adipose tissue (AT) is composed not only of adipocytes, but also of macrophages, endothelial cells and preadipocytes. Macrophages are an important component of AT, and are involved in tissue homeostasis, tissue repair and fibrosis. AT-resident macrophages are categorized into two subtypes, the M1-like and M2-like macrophages. M2-like macrophages are reported to play anti-inflammatory roles, and to be involved in clearing and removal of dying/dead adipocytes, and recruiting adipocyte progenitors (APs). M2-like macrophages are also reported to be involved in the promotion of fibrosis in a transforming growth factor-β-dependent manner. However, the precise roles of M2-like macrophages in the AT have not yet been clearly delineated. Recently, we generated genetically engineered transgenic mice in which CD206 + M2-like macrophages can be conditionally depleted. Unexpectedly, we found that the depletion of CD206 + M2-like macrophages resulted in the enhanced generation of smaller adipocytes, improved insulin sensitivity and proliferation of APs. We further clarified that the CD206 + M2-like macrophages directly interact with the APs to regulate their growth/differentiation and adipogenesis, thereby controlling adiposity and systemic insulin sensitivity. In the present review, we discuss how CD206 + M2-like macrophages provide a niche for APs and maintain glucose homeostasis.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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