论文部分内容阅读
目的探讨内毒素耐受对高果糖膳食引起的肝脏胰岛素抵抗发生的影响。方法昆明种小鼠随机分为对照组、果糖组、内毒素耐受组;对照组以普通饮食和自来水饲养,果糖组和内毒素耐受组饮食与对照组相同,但饮水改为20%果糖水,内毒素耐受组于高果糖饮水前3d连续腹腔注射LPS 2mg/kg后,以后隔日皮下注射LPS 0.1mg/kg,上述各实验组动物喂养12wk后,处死动物观察肝脏大体形态和组织学改变,检测空腹血糖(FPG)、空腹血胰岛素水平(FINS),计算胰岛素抵抗指数(FIRI)及肝脏胰岛素受体p-IRβ/IRβ、细胞因子信号转导抑制子(SOCS3)、白细胞介素-1受体相关激酶(IRAK-M)蛋白的表达。结果与对照组相比果糖组小鼠FBS、FIRI、肝指数均明显增高(P<0.05),而FINS与正常组相比也增高,无统计学意义;内毒素耐受组FPG、FINS、FIRI及肝指数均高于果糖组(P<0.05);肝脏p-IRβ/IRβ表达下调,SOCS3、IRAK-M表达上调,具有统计学差异(P<0.05),肝脂肪变情况明显加重。结论慢性小剂量内毒素诱导内毒素耐受可加重果糖所致肝脏胰岛素抵抗的发生。
Objective To investigate the effect of endotoxin tolerance on hepatic insulin resistance induced by high fructose diet. Methods Kunming mice were randomly divided into control group, fructose group and endotoxin tolerant group. The control group was fed with normal diet and tap water. The diet of fructose group and endotoxin tolerant group was the same as the control group, but the drinking water was changed to 20% fructose Water and endotoxin tolerated group were given intraperitoneal injection of LPS 2mg / kg three days before high fructose drinking water and then injected with LPS 0.1mg / kg subcutaneously every other day. The animals in each experimental group were sacrificed for 12 weeks and then sacrificed to observe the gross morphology and histology (FPG), fasting blood insulin (FINS), insulin resistance index (FIRI), hepatic insulin receptor p-IRβ / IRβ, SOCS3 and interleukin- 1 receptor-associated kinase (IRAK-M) protein expression. Results Compared with the control group, the FBS, FIRI and liver index of mice in fructose group were significantly increased (P <0.05), and the levels of FINS in normal mice were also increased (P <0.05). The liver p-IRβ / IRβ expression was down-regulated and SOCS3 and IRAK-M were up-regulated with statistical significance (P <0.05). Conclusion Chronic low-dose endotoxin induced endotoxin tolerance may aggravate hepatic insulin resistance induced by fructose.