The functional induction of brown-like adipocytes in white adipose tissue (WAT) provides a defense against obesity. The aim of this study was to analyze the effects of milk fat globule membrane (MFGM) and its component phosphatidylcholine (PC) on the brown remodeling of WAT. Male C57BL/6 J mice were fed a high-fat diet (HFD) for 8 weeks and then fed HFD for another 8 weeks with MFGM. In vitro studies were performed in C3H10T1/2 pluripotent stem cells, 3T3-L1 pre-adipocytes and differentiated inguinal WAT stromal vascular cells (SVCs) to determine the role of MFGM and PC on the formation of brown-like adipocytes. MFGM decreased fasting glucose and serum insulin levels in HFD-fed mice. MFGM improved glucose tolerance and insulin sensitivity, and induced browning of inguinal WAT. MFGM and its component PC stimulated transformation of brown-like adipocytes in C3H10T1/2 pluripotent stem cells, 3T3-L1 adipocytes and SVCs by increasing the protein expression of UCP1, PGC-1α, PRDM16 as well as the mRNA expression of other thermogenic genes and beige cell markers. MFGM and PC also increased mitochondrial DNA (mtDNA) copy number, mitochondrial density and oxygen consumption rate and up-regulated the mRNA expression of mitochondria-biogenesis-related genes in vitro. PPARα inhibitor GW6471 treatment or knockdown of PPARα using lentivirus-expressing shRNA inhibited the PC-induced increase in the protein expression of UCP1, PGC-1α and PRDM16 in C3H10T1/2 pluripotent stem cells and 3T3-L1 adipocytes, indicating the potential role of PPARα in PC-mediated brown-like adipocyte formation. In conclusion, MFGM and milk PC induced adipose browning, which has major protective effects against obesity and metabolic dysfunction.

白色脂肪组织（WAT）中褐色样脂肪细胞的功能诱导提供了对抗肥胖的防御作用。这项研究的目的是分析乳脂球膜（MFGM）及其成分磷脂酰胆碱（PC）对WAT棕色重塑的影响。给雄性C57BL / 6 J小鼠喂食高脂饮食（HFD）8周，然后再用MFGM喂食HFD 8周。体外研究人员在C3H10T1 / 2多能干细胞，3T3-L1前脂肪细胞和分化的腹股沟WAT基质血管细胞（SVC）中进行了研究，以确定MFGM和PC在褐色脂肪细胞形成中的作用。MFGM降低了喂食HFD的小鼠的空腹血糖和血清胰岛素水平。MFGM改善了葡萄糖耐量和胰岛素敏感性，并导致腹股沟WAT褐变。MFGM及其成分PC通过增加UCP1，PGC-1α，PRDM16的蛋白质表达以及其他产热基因的mRNA表达来刺激C3H10T1 / 2多能干细胞，3T3-L1脂肪细胞和SVC中褐色样脂肪细胞的转化。米色细胞标记。MFGM和PC也增加了线粒体DNA（mtDNA）的拷贝数，体外。PPARα抑制剂GW6471处理或使用表达慢病毒的shRNA抑制PPARα抑制PC诱导的C3H10T1 / 2多能干细胞和3T3-L1脂肪细胞中UCP1，PGC-1α和PRDM16蛋白表达的增加，表明PPARα的潜在作用在PC介导的褐色样脂肪细胞形成中。总之，MFGM和牛奶PC诱导脂肪褐变，对肥胖和代谢功能障碍具有重要的保护作用。