乳铁蛋白调节高脂饮食小鼠糖脂代谢的机制

目的:探究乳铁蛋白(LF)调节高脂饮食引起的小鼠糖脂代谢紊乱的机制。方法:选取30只SPF级雄性C57BL/6小鼠随机分为对照组(K组，正常饮食)、模型组(M组，高脂饲料+饮纯水)、乳铁蛋白治疗组(Y2组，高脂饲料+饮2%乳铁蛋白水)，连续喂养12周。每周记录小鼠体质量变化。在第12周取附睾周围腹腔脂肪组织，测定内脏脂肪率。使用商业酶分析试剂盒测血糖、血脂水平，酶联免疫吸附法测定胰岛素水平，16S rRNA测序法检测小鼠的肠道菌群，气相色谱质谱法检测短链脂肪酸含量。结果:乳铁蛋白干预12周后，Y2组小鼠相比于M组小鼠内脏脂肪率下降31.05%，血糖(5.92 mmol/L)、胰岛素(19.60 mmol/L)、总胆固醇(3.17 mmol/L)、甘油三酯(0.28 mmol/L)和低密度脂蛋白水平(1.84 mmol/L)与M组相比均下降且差异显著(P＜0.05)，高密度脂蛋白水平(1.88 mmol/L)与M组相比显著上升(P＜0.05)。乳铁蛋白干预降低了厚壁菌门和拟杆菌门的比值，增加了拟杆菌门的相对丰度，降低了颤螺旋菌、大肠埃希菌、脱铁杆菌的相对丰度，调节了短链脂肪酸的代谢异常，控制了脂肪的积累。结论:乳铁蛋白通过调节肠道菌群结构来调控脂肪积累，改善高脂饮食小鼠的糖脂代谢紊乱。

Mechanism of Lactoferrin in Regulating Glycolipid Metabolism in High-fat Diet Mice

Objective: To investigate the mechanism of lactoferrin(LF) regulating the disorder of glucose and lipid metabolism in mice induced by high-fat diet. Methods: Thirty SPF grade male C57BL/6 mice were randomly divided into a control group (Group K， normal diet)， model group (Group M， high-fat diet drinking pure water)， and LF treatment group (Group Y2， high-fat diet drinking 2% lactoferrin water). The mice were fed continuously for 12 weeks. Body weight changes of the mice were recorded weekly. Visceral fat percentage was measured at week 12 by taking peri-epididymal abdominal adipose tissue. Blood glucose and lipid levels were analyzed using commercial enzymatic assay kits. Insulin levels were measured using ELISA. 16S rRNA sequencing was used to measure the intestinal flora of the mice. Short-chain fatty acids were detected by gas chromatography-mass spectrometry. Results: After 12 weeks of lactoferrin intervention， the visceral fat percentage of mice in Y2 group decreased by 31.05% compared with mice in M group. Blood glucose (5.92 mmol/L)， insulin (19.60 mmol/L), total cholesterol (3.17 mmol/L)， triglyceride (0.28 mmol/L)， low density lipoprotein (1.84 mmol/L) levels were all decreased and the differences were significant compared with group M (P<0.05). The high density lipoprotein level (1.88 mmol/L) was significantly increased compared with that of group M (P<0.05). Lactoferrin intervention decreased the ratio of Firmicutes/Bacteroidetes and increased the relative abundance of Bacteroidetes， decreased the relative abundance of Colidextribacter and Deferribacteres， regulated the abnormal metabolism of short-chain fatty acids， and controlled the accumulation of fat. Conclusions: Lactoferrin regulates the accumulation of fat by regulating the structure of intestinal flora， and improves the disorder of glucose and lipid metabolism in high-fat diet mice.