Regular exercise is the first line of therapy for treating obesity-mediated metabolic disorders, including insulin resistance. It has been reported that developmental endothelial locus-1 (DEL-1) enhances macrophage efferocytosis, resulting in inflammation clearance as well as improves insulin resistance in skeletal muscle. However, the relationship between exercise and DEL-1, and the effects of DEL-1 on insulin signalling in adipocytes have not been fully elucidated to date. Protein expression levels were determined by Western blot analysis. Cells were transfected with small interfering (si) RNA to suppress gene expression. Lipid accumulation levels were detected using Oil red-O staining. Proinflammatory cytokine secretion levels were measured using ELISA. DEL-1 expression levels were induced in the skeletal muscle of people who exercised using microarray analysis. Recombinant DEL-1 augmented AMP-activated protein kinase (AMPK) phosphorylation and haem oxygenase (HO)-1 expression to alleviating inflammation and impairment of insulin signalling in 3T3-L1 adipocytes treated with palmitate. siRNA of AMPK or HO-1 also mitigated the effects of DEL-1 on inflammation and insulin resistance. DEL-1 ameliorates inflammation and insulin resistance in differentiated 3T3-L1 cells via AMPK/HO-1 signalling, suggesting that DEL-1 may be the exercise-mediated therapeutic target for treating insulin resistance and type 2 diabetes.

定期运动是治疗肥胖介导的代谢紊乱（包括胰岛素抵抗）的第一线疗法。据报道，发育性内皮基因座1（DEL-1）增强了巨噬细胞的胞吞作用，导致炎症清除，并改善了骨骼肌的胰岛素抵抗。然而，迄今为止，尚未完全阐明运动与DEL-1之间的关系以及DEL-1对脂肪细胞中胰岛素信号的影响。通过蛋白质印迹分析确定蛋白质表达水平。用小的干扰（si）RNA转染细胞以抑制基因表达。使用油红O染色检测脂质积累水平。使用ELISA测量促炎细胞因子的分泌水平。使用微阵列分析在运动人群的骨骼肌中诱导了DEL-1表达水平。重组DEL-1增强了AMP活化的蛋白激酶（AMPK）磷酸化和血红素加氧酶（HO）-1的表达，从而减轻了用棕榈酸酯处理的3T3-L1脂肪细胞的炎症和胰岛素信号传导的损伤。AMPK或HO-1的siRNA也减轻了DEL-1对炎症和胰岛素抵抗的影响。DEL-1通过AMPK / HO-1信号改善了分化的3T3-L1细胞的炎症和胰岛素抵抗，提示DEL-1可能是运动介导的治疗靶点，可治疗胰岛素抵抗和2型糖尿病。重组DEL-1增强了AMP活化的蛋白激酶（AMPK）磷酸化和血红素加氧酶（HO）-1的表达，从而减轻了用棕榈酸酯处理的3T3-L1脂肪细胞的炎症和胰岛素信号传导的损伤。AMPK或HO-1的siRNA也减轻了DEL-1对炎症和胰岛素抵抗的影响。DEL-1通过AMPK / HO-1信号改善了分化的3T3-L1细胞的炎症和胰岛素抵抗，提示DEL-1可能是运动介导的治疗靶点，可治疗胰岛素抵抗和2型糖尿病。重组DEL-1增强了AMP活化的蛋白激酶（AMPK）磷酸化和血红素加氧酶（HO）-1的表达，从而减轻了用棕榈酸酯处理的3T3-L1脂肪细胞的炎症和胰岛素信号传导的损伤。AMPK或HO-1的siRNA也减轻了DEL-1对炎症和胰岛素抵抗的影响。DEL-1通过AMPK / HO-1信号改善了分化的3T3-L1细胞的炎症和胰岛素抵抗，提示DEL-1可能是运动介导的治疗靶点，可治疗胰岛素抵抗和2型糖尿病。