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目的探讨高脂诱导肥胖大鼠血脂、血糖及血浆中脂肪细胞因子水平与骨代谢因子的相关性。方法 5~6周龄Wistar健康雄性大鼠,随机分为普通饲料(对照组)和高脂饲料(实验组),连续喂养14周,诱导大鼠肥胖模型。分别于第0、4、6、8、10周每组选取8只,空腹麻醉后眼底静脉取血并分离血浆,测定血浆甘油三酯(TG)、总胆固醇(TC)、游离脂肪酸(FFA)、葡萄糖(Glu)、低密度脂蛋白(LDL)和高密度脂蛋白(HDL)水平;酶联免疫法测定血浆中肿瘤坏死因子-α(TNF-α)、核因子NF-κB受体活化因子配体(RANKL)、核因子κB受体活化因子(RANK)、瘦素(LPT)及脂联素(APN)水平。结果喂养4周后,2组大鼠体重差异开始有统计学意义(P<0.05),实验组显著高于对照组。至第10周,2组大鼠体重均进入平台期,体重不再增加,但2组差异仍有统计学意义(P<0.01),实验组仍高于对照组。实验组大鼠血浆中Glu、FFA、TG、TC、LDL、TNF-α、RANKL、RANK、LPT水平始终高于对照组大鼠,而APN水平低于正常大鼠,差异有统计学意义(P<0.05);大鼠血浆中骨代谢因子RANKL与TNF-α、FFA、TG显著正相关(r值分别为0.412、0.270、0.321,P值均<0.05),RANK与TNF-α、FFA、TG及LPT显著正相关(r值分别为0.392、0.270、0.326,0.271,P值均<0.05)。结论肥胖状态下大鼠血脂代谢紊乱可通过影响脂肪细胞因子APN及LPT水平始动炎症发生,而炎症状态下高水平TNF-α通过影响RANKL及RANK导致骨代谢异常。
Objective To investigate the relationship between serum lipid, blood glucose and adipokines in hyperlipemia-induced obese rats and bone metabolism. Methods Wistar healthy male rats (5 to 6 weeks old) were randomly divided into normal diet (control group) and high-fat diet (experimental group), and were fed for 14 weeks continuously to induce obesity model in rats. Eight rabbits in each group were selected at the 0th, 4th, 6th, 8th and 10th weeks respectively. After fasting anesthesia, the blood was taken from the fundus and plasma was separated. Plasma triglyceride (TG), total cholesterol (TC), free fatty acid (FFA) (Glu), low density lipoprotein (LDL) and high density lipoprotein (HDL) were determined by enzyme-linked immunosorbent assay. The levels of tumor necrosis factor-α (TNF- RANKL, RANK, LPT and APN. Results Four weeks after feeding, the body weight of the two groups began to have statistical significance (P <0.05), and the experimental group was significantly higher than the control group. At the 10th week, the body weight of the rats in both groups entered the plateau, the body weight no longer increased, but the differences between the two groups were still statistically significant (P <0.01). The experimental group was still higher than the control group. The levels of Glu, FFA, TG, TC, LDL, TNF-α, RANKL, RANK and LPT were all higher in the experimental group than those in the control group, while the level of APN was lower than that in the normal group (P <0.05). There was a significant positive correlation between RANKL and TNF-α, FFA, TG (r = 0.412,0.270,0.321, P <0.05) And LPT (r values were 0.392,0.270,0.326,0.271, P values were <0.05). CONCLUSION: The disorder of lipid metabolism in obese rats can initiate inflammation by affecting APN and LPT levels of adipocytes, whereas high level of TNF-α in inflammatory state can lead to abnormal bone metabolism by affecting RANKL and RANK.