高果糖、高脂喂养致小鼠肝脏内质网应激的时程变化

发布时间：2018-02-13 16:02

本文关键词： 甘油三酯脂肪肝内质网应激　出处：《中国老年学杂志》2015年23期 　论文类型：期刊论文

【摘要】：目的探讨高果糖与高脂饮食对比诱导的小鼠肝脏内质网应激(ERS)的发生时程变化。方法雄性C57BL/J6小鼠分为对照组、高果糖组及高脂组,分别在喂养3 d、8 w后测定各组小鼠空腹血糖(FPG)、空腹血清胰岛素(FINS)、肝脏甘油三酯(TG)含量,并测定各组小鼠肝脏ERS标志物——磷酸化胰腺内质网激酶(p-PERK)及磷酸化山梨醇要求激酶-1(p-IRE1/t-IRE1)的蛋白表达。结果喂养3 d后,与对照组相比,两组FPG、FINS无明显变化,而肝TG水平均显著增加;喂养8 w后,与对照组相比,两组FPG、FINS、肝TG水平均显著增加;喂养3 d后,与对照组相比,高果糖组的肝内p-PERK、p-IRE1蛋白表达显著增加,提示出现ERS,而高脂组GRP78、p-PERK的蛋白表达与对照组无显著区别;喂养8 w后,高果糖、高脂组的肝内p-PERK、p-IRE1蛋白表达均显著增加。结论短期和长期高果糖和高脂喂养均可引起肝内脂质沉积,但高果糖喂养小鼠在脂肪肝发生早期即可出现肝ERS,而高脂喂养小鼠则在长期喂养后方出现肝ERS,提示ERS与高果糖、高脂饮食诱导的脂肪肝发生发展均有关,但介导机制不同。
[Abstract]:Objective to investigate the time course of endoplasmic reticulum stress (ERS) induced by high fructose and high fat diet in mice. Methods male C57BL / J6 mice were divided into three groups: control group, high fructose group and high fat group. After feeding for 3 days and 8 weeks, the contents of fasting blood glucose (FPG), fasting serum insulin (FINSN) and hepatic triglyceride (TG) were measured in each group. The expression of phosphorylated pancreatic endoplasmic reticulum kinases (p-PERK) and phosphorylated sorbitol required kinases (-1pIRE1 / t-IRE1) in the liver of mice in each group were determined. Results after 3 days of feeding, there was no significant change in the expression of ERS in the two groups as compared with that in the control group. After 8 weeks of feeding, compared with the control group, the levels of liver TG and FPGfins were significantly increased, and after 3 days of feeding, the expression of p-PERKPERKP- IRE1 protein in the liver of high fructose group was significantly higher than that in the control group, and that in the high fructose group was significantly higher than that in the control group. The results indicated that the expression of GRP78 p-PERK in hyperlipidemia group was not significantly different from that in control group, and the expression of GRP78 p-PERK protein in hyperfructose group was higher than that in control group after 8 weeks of feeding. The expression of p-PERKN p-IRE1 protein was significantly increased in hyperlipidemia group. Conclusion both short and long term high fructose and high fat feeding can induce lipid deposition in liver. However, high fructose fed mice could develop liver ERS at the early stage of fatty liver, while high fat feeding mice had liver ERS after long-term feeding, suggesting that ERS was related to high fructose and high fat diet induced fatty liver development, but the mediating mechanism was different.
【作者单位】：河北省人民医院内分泌一科;
【基金】：国家自然基金资助项目(No.81200639)
【分类号】：R575.5

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