Objective To investigate the effect of concurrent exercise intervention in metabolic endotoxemia induced by high-fat diet in rats,and further understand the damage of liver mitochondrial ultramicrostructure.Methods Eighteen SD rats with the weight of 100g were randomly divided into 3 groups:group A (standard diet group),group B(high-fat diet group) and group C (treadmill-trained group with high-fat diet).Training (1 hour/d) initiated at the same time as the HF diet was fed.After being raised for 6 weeks,the rats was euthanized and weighed up.Blood samples were taken and the levels of serum lipid were detected.The levels of serum endotoxin were detected by enzyme-linked immunoadsorbent assay.The membrane potentials of isolated mitochondrion were detected by flow cytometry instrument and the morphologic changes in mitochondria in liver were observed by electronic microscopy.Results In group B,the levels of endotoxin increased significantly(2.916 ± 0.761 rs 5.454 ± 1.254,t =-4.236,P ＜ 0.05),and the liver mitochondrial density and membrane potential also increased significantly compared with group A after 6 weeks (4.330 ±0.501 vs 3.507 ±0.532,t =2.759,P ＜0.05;l.660 ±0.202 vs 0.473 ±0.064,t =13.712,P ＜0.05).But there was no markedly different in serum endotoxin between group B and group C (4.972 ± 1.757 vs 5.454 ± 1.254,t =-0.547,P ＞ 0.05).Compared with group B,the liver mitochondrial density of group C decreased significantly (4.330±0.501 vs 3.581 ±0.188,t =3.426,P ＜ 0.05).The mitochondrial ultrastructurctural changes in each group were not obvious.Conclusions The rats fed with high-fat diet for 6 weeks can reach the state of metabolic endotoxemia.The increasing levels of the liver mitochondrial membrane potential caused by metabolic endotoxin may affect the happening and development of other diseases in the future.Concurrent exercise can not decrease the level of endotoxin.It also shows that metabolic disease caused by high-fat diet should be prevented by moderation in eating and drinking.%目的 研究早期运动干预对于高脂饮食诱导代谢性内毒素血症的影响,了解其对线粒体形态功能的改变.方法 将100g左右的SPF级SD雄鼠随机分为A组(正常饮食组)、B组(高脂饮食组)及C组(高脂饮食联合运动组) . 于清洁级环境中饲养6周后处死,检测其体质量、血脂、血清内毒素水平.透射电镜了解其肝脏超微结构变化.差速离心法提取肝脏线粒体后,流式细胞仪检测其肝脏线粒体肿胀度及线粒体膜电位.结果 饲养6周后,大鼠内毒素水平,B组相对于A组差异有统计学意义(2.916 ±0.761比5.454±1.254,t=-4.236,P＜0.05);透射电镜下观察B组细胞中的脂滴,较A、C组明显增多.但C组血清内毒素水平与B组比较,差异无统计学意义(4.972±1.757比5.454±1.254,t=-0.547,P ＞0.05).比较各组大鼠肝脏线粒体肿胀情况,B组相对于A、C组,差异均有统计学意义(4.330±0.501比3.507±0.532,t =2.759,P＜0.05;4.330±0.501比3.581±0.188,t=3.426,P＜0.05) . 各组大鼠肝脏线粒体膜电位情况,B、C组和A组比较,差异均有统计学意义(1.660±0.202比0.473±0.064,t=13.712,P ＜0.05;2.012±0.506比0.473±0.064,t=7.411,P ＜0.05).但各组透射电镜中线粒体形态并没有出现显并性差异.结论 大鼠经高脂饮食喂养6周后可出现代谢性内毒素血症状态.代谢性内毒素对肝脏线粒体膜电位水平的影响,说明代谢性内毒素血症可能对未来疾病的发生发展产生影响.早期运动干预对循环中内毒素水平无明显影响,也从侧面说明高脂饮食所带来的危害并不能单纯通过运动来控制,合理膳食对于青少年键康尤其重要.
展开▼
