The study investigates the mechanism by which adipose tissue macrophages (ATMs) switch from an alternatively activated (M2a) to a classically activated (M1) phenotype in obesity. Using C57Bl/6 mice, the researchers found that resident ATMs in lean mice express the M2a marker macrophage galactose N-acetyl-galactosamine specific lectin 1 (MGL1) and localize to interstitial spaces between adipocytes. In obese mice, MGL1+ ATMs remain in these spaces, while a population of MGL1-CCR2+ ATMs with high M1 and low M2a gene expression is recruited to clusters surrounding necrotic adipocytes. Pulse labeling showed that the recruitment rate of new macrophages to MGL1- ATM clusters is significantly faster than that of interstitial MGL1+ ATMs, and this recruitment is attenuated in Ccr2-/- mice. M2a- and M1-polarized macrophages produced different effects on adipogenesis and adipocyte insulin sensitivity in vitro. The study concludes that the shift in the M2a/M1 ATM balance is generated by spatial and temporal differences in the recruitment of distinct ATM subtypes, rather than the conversion of resident M2a macrophages to M1 ATMs in situ.The study investigates the mechanism by which adipose tissue macrophages (ATMs) switch from an alternatively activated (M2a) to a classically activated (M1) phenotype in obesity. Using C57Bl/6 mice, the researchers found that resident ATMs in lean mice express the M2a marker macrophage galactose N-acetyl-galactosamine specific lectin 1 (MGL1) and localize to interstitial spaces between adipocytes. In obese mice, MGL1+ ATMs remain in these spaces, while a population of MGL1-CCR2+ ATMs with high M1 and low M2a gene expression is recruited to clusters surrounding necrotic adipocytes. Pulse labeling showed that the recruitment rate of new macrophages to MGL1- ATM clusters is significantly faster than that of interstitial MGL1+ ATMs, and this recruitment is attenuated in Ccr2-/- mice. M2a- and M1-polarized macrophages produced different effects on adipogenesis and adipocyte insulin sensitivity in vitro. The study concludes that the shift in the M2a/M1 ATM balance is generated by spatial and temporal differences in the recruitment of distinct ATM subtypes, rather than the conversion of resident M2a macrophages to M1 ATMs in situ.