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目的 : 探讨下丘脑腹内侧核损伤性肥胖大鼠脂肪肝形成机制。方法 : 雌性 SD大鼠分为下丘脑腹内侧核损伤肥胖组 (VMH)和下丘脑腹内侧核非损伤对照组 (sham) ,于下丘脑腹内侧核损伤和伪性损伤 1 w后 ,留取肝脏作形态学观察和测定肝脏甘油三酯、磷脂酰磷酸水解酶、苹果酸酶、葡萄糖 - 6 -磷酸脱氢酶及微粒体甘油三酯转运蛋白活性。结果 : VMH组大鼠肝脏中甘油三酯的含量明显增高 ,是对照组的 1 .8倍 ,肝脏磷脂酰磷酸水解酶、苹果酸酶、葡萄糖 - 6 -磷酸脱氢酶活性均高于对照组。显微镜下 ,在 VMH肥胖组大鼠肝细胞中可见有大量的脂质颗粒 ,而其对照组肝细胞中并没有见到类似的脂质颗粒。 VMH肥胖组大鼠肝细胞的微粒体甘油三酯转运蛋白活性是对照组的 1 .1 5倍 ,而且肝脏微粒体甘油三酯转运蛋白活性与血浆胰岛素水平呈明显的相关关系 (R=0 .86 3 ,P<0 .0 5 )。结论 : VMH肥胖大鼠肝脏甘油三酯的产生和微粒体甘油三酯转运蛋白活性均明显增高 ,但后者的增加程度明显低于前者 ,这样可能导致肝脏中产生的甘油三酯不能被微粒体甘油三酯转运蛋白及时从肝脏转运出去 ,而导致甘油三酯在肝脏中积累形成脂肪肝。
Objective: To investigate the mechanism of fatty liver formation in the hypothalamic ventricle of instrified rats. Methods: Female Sprague-Dawley rats were randomly divided into two groups: the hypothalamic VMH group and sham non-injury control group of hypothalamic ventrolateral medulla. Liver morphology was observed and liver triglyceride, phosphatidylcholine hydrolase, malic enzyme, glucose - 6 - phosphate dehydrogenase and microsomal triglyceride transporter activity was measured. Results: The content of triglyceride in the liver of VMH group was significantly increased, which was 1.8 times that of the control group, and the activities of liver phosphatidylcholine hydrolase, malic enzyme and glucose - 6 - phosphate dehydrogenase were higher than those of the control group . Under the microscope, a large number of lipid particles were seen in the liver cells of VMH obese rats, and no similar lipid particles were seen in the control liver cells. The activity of microsomal triglyceride transporter in liver cells of VMH obese rats was 11.5 times that of the control group, and the activity of hepatic microsomal triglyceride transporters was positively correlated with plasma insulin level (R = 0. 86 3, P <0. 05). CONCLUSIONS: Both hepatic triglyceride production and microsomal triglyceride transporter activity in VMH obese rats were significantly increased, but the latter increased significantly less than the former, which may result in triglycerides produced in the liver not being metabolized by microsomes Triglyceride transporters are promptly transported out of the liver, resulting in the accumulation of triglycerides in the liver to form fatty liver.