大鼠认知障碍对糖代谢的影响及其与肝脏和骨骼肌糖原合成酶激酶-3β表达水平的关系

Eeffects of cognitive impairment in rats on glucose metabolism and its relations with expression of GSK-3β in liver and skeletal muscle

摘要:

目的  探讨大鼠认知障碍对糖代谢的影响及其与肝脏和骨骼肌；糖原合成酶激酶-3β（GSK-3β）表达的关系，为糖代谢的神经调节机制研究提供新的实验依据。方法  Aβ1-42大鼠海马内注射构建认知障碍模型，血糖仪检测大鼠空腹血糖（FPG），半定量反转录-聚合酶链反应法（RT-PCR）检测肝脏与骨骼肌GSK-3β mRNA的表达，蛋白印迹法（Western blot）检测肝脏与骨骼肌GSK-3β的表达。结果  ①实验组大鼠FPG为（7.99±0.15）mmol/L，与假手术组和对照组比较显著升高（P <0.05）。②实验组大鼠肝脏和骨骼肌GSK-3β mRNA表达水平分别为（0.47±0.03）和（0.26±0.02），与假手术组和对照组比较均明显升高（P < 0.05）。③实验组大鼠肝脏和骨骼肌GSK-3β表达水平分别为（0.47±0.04）和（0.26±0.03），均显著高于假手术组与对照组（P <0.05）。结论  大鼠认知障碍可引起血糖水平的升高，其机制可能与认知障碍大鼠肝脏和骨骼肌GSK-3β表达升高有关。

Abstract:

Objective To investigate the effects of cognitive impairment in rats on glucose metabolism and its relation with the expression of GSK-3β in liver and skeletal muscle, and to provide a new experimental evidence for study of the neural mechanisms regulating glucose metabolism. Methods The Aβ1-42 was injected into the hippocampus to build cognitive impairment model of rats, and fasting blood glucose of rats was tested by blood glucose meter. Expression of GSK-3βmRNA and GSK-3β in liver and skeletal muscle were detected by RT-PCR and Western blot, respectively. Results In the experimental group, fasting blood glucose (FPG) was (7.99 ± 0.15) mmol/L, which was significantly higher than that in the sham group and the control group (P < 0.05). The expressions of GSK-3β mRNA in liver and skeletal muscle of the experimental group were (0.47 ± 0.03) and (0.26 ± 0.02), which were significantly higher than other two groups (P < 0.05). The expressions of GSK-3β in liver and skeletal muscle of the experimental group were (0.47 ± 0.04) and (0.26 ± 0.03), which also higher than other groups significantly (P < 0.05). Conclusions Cognitive impairment in rats causes the elevation of glucose levels, which mechanism may related to the increase of expression of GSK-3β in liver and skeletal muscle.