Obesity induces a phenotypic switch in adipose tissue macrophages (ATMs) from an anti-inflammatory M2 state to a proinflammatory M1 state. In lean mice, ATMs express genes characteristic of M2 polarization, such as Ym1, arginase 1, and Il10, which protect adipocytes from inflammation. In contrast, diet-induced obesity leads to increased expression of proinflammatory genes like Tnfa and Nos2, and decreased expression of anti-inflammatory genes. A novel F4/80+CD11c+ population of ATMs is identified in obese mice, which may contribute to the proinflammatory state. CCR2-KO mice, which have reduced ATM content and improved insulin sensitivity, retain M2 markers at levels similar to lean mice. IL-10, an antiinflammatory cytokine, protects adipocytes from TNF-α-induced insulin resistance by activating STAT3 and PI3K pathways. The study suggests that the shift from M2 to M1 polarization in ATMs is a key factor in the development of insulin resistance in obesity.Obesity induces a phenotypic switch in adipose tissue macrophages (ATMs) from an anti-inflammatory M2 state to a proinflammatory M1 state. In lean mice, ATMs express genes characteristic of M2 polarization, such as Ym1, arginase 1, and Il10, which protect adipocytes from inflammation. In contrast, diet-induced obesity leads to increased expression of proinflammatory genes like Tnfa and Nos2, and decreased expression of anti-inflammatory genes. A novel F4/80+CD11c+ population of ATMs is identified in obese mice, which may contribute to the proinflammatory state. CCR2-KO mice, which have reduced ATM content and improved insulin sensitivity, retain M2 markers at levels similar to lean mice. IL-10, an antiinflammatory cytokine, protects adipocytes from TNF-α-induced insulin resistance by activating STAT3 and PI3K pathways. The study suggests that the shift from M2 to M1 polarization in ATMs is a key factor in the development of insulin resistance in obesity.