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目的:探讨髓源性生长因子（MYDGF）对肥胖小鼠白色脂肪棕色化的影响。方法:高脂饲料喂养雄性C57BL/6J野生型（WT）小鼠和MYDGF基因敲除（KO）小鼠12周，根据使用腺相关病毒（AAV）-MYDGF或AAV-绿色荧光蛋白（GFP）干预，将WT和KO小鼠分为WT-GFP组、WT-MYDGF组、KO-GFP组和KO-MYDGF组，普通饲料喂养的WT小鼠作为对照组。收集各组小鼠的体重、日间和夜间产热量，解剖分离各组小鼠两侧附睾白色脂肪组织（eWAT）、腹股沟白色脂肪组织（iWAT）和肩胛棕色脂肪组织（iBAT）并称重，HE染色观察脂肪细胞形态，免疫组化和实时荧光定量聚合酶链反应（RT-PCR）检测皮下脂肪棕色化相关基因［解偶联蛋白1（n UCP1）、过氧化物酶体增殖物激活受体γ（n PPARγ）、过氧化物酶体增殖物激活受体γ共激活因子1α（n PGC-1α）、PR结构域蛋白16（n PRDM16）］的表达，免疫荧光检测皮下脂肪血管数量。根据噻唑蓝（MTT）实验结果，选择使用100 ng/ml重组MYDGF（rMYDGF）干预24 h的3T3-L1细胞作为实验（rMYDGF）组，未进行rMYDGF干预的细胞培养24 h作为对照（Vehicle）组，采用RT-PCR和Western blot法检测两组细胞UCP1、PPARγ、PGC-1α、PRDM16的mRNA和蛋白的表达水平。采用独立样本n t检验比较组间差异。n 结果:共纳入30只小鼠，对照组、WT-GFP组、WT-MYDGF组、KO-GFP组和KO-MYDGF组各6只。干预12周后，与WT-GFP组和KO-GFP组相比，WT-MYDGF组与KO-MYDGF组小鼠体重均降低，日间和夜间产热能力均提高，n UCP1、n PPARγ、n PGC-1α、n PRDM16的mRNA表达水平和血管数量均增高（n P<0.05），小鼠eWAT和iWAT的体积和细胞均减小；与WT-GFP组相比，WT-MYDGF组的eWAT和iWAT重量均减小（n P<0.05）；与KO-GFP组相比，KO-MYDGF组的eWAT重量减小（n P<0.05）。体外培养3T3-L1脂肪细胞并使用重组MYDGF干预的结果显示，与Vehicle组相比，rMYDGF干预组的棕色化相关基因UCP1、PPARγ、PGC-1α、PRDM16的mRNA和蛋白的表达水平均增高（n P<0.05）。n 结论:MYDGF可促进肥胖小鼠白色脂肪棕色化。“,”Objective:To investigate the effect of myeloid-derived growth factor (MYDGF) on browning of white adipose tissue in obese mice.Methods:Male C57BL/6J wild-type (WT) mice and MYDGF knockout (KO) mice fed a high fat diet for 12 weeks were divided into WT-GFP group, WT-MYDGF group, KO-GFP group, and KO-MYDGF group according to AAV (adeno-associated viral)-MYDGF or AAV-GFP (green fluorescent protein) intervention. WT mice fed a normal chow diet were used as a control group. The body weight and heat production during the light and dark of mice in each group were detected. The epididymal white adipose tissue (eWAT), the inguinal white adipose tissue (iWAT) and the interscapular brown adipose tissue (iBAT) were isolated and weighed. The morphology of adipocytes was observed by hematoxylin and eosin (HE) staining. The expression of browning-related genes [uncoupling protein 1 (n UCP1), peroxisome proliferator-activated receptor γ (PPARγ), peroxisome proliferator-activated receptor γ coactivator-1α (n PGC-1α), PRD1-BF1-RIZ1 homologous domain containing 16 (n PRDM16)] were detected by immunohistochemistry and the real-time polymerase chain reaction (RT-PCR), the vessels of adipose tissues were detected by immunofluorescence staining in subcutaneous adipose tissue. According to the results of MTT experiment, 3T3-L1 preadipocytes treated with 100 ng/ml recombinant MYDGF (rMYDGF) for 24 h were selected as experimental group (rMYDGF), and cells treated with 0 ng/ml rMYDGF for 24 h were selected as control group (Vehicle). The mRNA and protein expression levels of UCP1, PPARγ, PGC-1α and PRDM16 were detected by RT-PCR and western blot. Independent-samples n t test was used for comparison between two groups.n Results:A total of 30 mice were enrolled, including 6 mice in each of the control group, WT-GFP group, WT-MYDGF group, KO-GFP group and KO-MYDGF group. After 12 weeks of intervention, the body weight of WT-MYDGF group and KO-MYDGF group decreased compared with WT-GFP group and KO-GFP group, while heat production during the light and dark increased, the mRNA expression of n UCP1, n PPARγ, n PGC-1α, n PRDM16 and the number of blood vessels increased (n P<0.05). The volume and cell size of eWAT and iWAT decreased in mice supplemented with MYDGF. The weight of eWAT and iWAT decreased in WT-MYDGF group compared with WT-GFP group (n P<0.05), and the weight of eWAT decreased in KO-MYDGF group compared with KO-GFP group (n P<0.05). In vitro, the mRNA and protein expression of browning-related genes UCP1, PPARγ, PGC-1α and PRDM16 increased in 3T3-L1 adipocytes of rMYDGF group compared with Vehicle group (n P<0.05).n Conclusion:MYDGF promotes browning of white adipose tissue in obese mice.