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目的探讨小鼠糖负荷后血糖的变化与下丘脑腹内侧核神经元表达PGC-1α变化之间的关系。方法昆明小鼠禁食禁水过夜后,随机分为空腹对照组、灌胃50%葡萄糖(2 g/kg)30、60、120和180 min组。分别于观察时间点尾静脉血糖测试结果,并利用免疫组织化学方法半定量观察小鼠下丘脑腹内侧核PGC-1α阳性细胞的变化。结果糖负荷结果:与空腹对照组相比,糖负荷后血糖开始升高,30 min组血糖水平最高,之后开始下降,180 min组降至糖负荷前水平。分别为7.25±2.84(对照组)、16.22±3.51(30 min组)、14.08±4.14(60 min组)、12.07±1.85(120 min组)、10.12±1.31 mmol/L(180 min组)。免疫组化结果:与空腹对照组相比,糖负荷后各组腹内侧核PGC-1α阳性神经细胞数量均显著性降低(P<0.05);糖负荷120 min组最低,之后开始恢复。相关性分析显示血糖水平与下丘脑腹内侧核PGC-1α阳性神经细胞数变化之间有显著的相关性(r=0.983)。结论在小鼠糖负荷实验过程中,血糖升高与下丘脑腹内侧核神经元PGC-1表达下调之间显著相关,提示下丘脑PGC-1表达可能是维持血糖稳定的环节之一。
Objective To investigate the relationship between the changes of blood glucose and the expression of PGC-1α in hypothalamic ventromedial neurons after the mice are loaded with glucose. Methods Kunming mice were fasted overnight and were randomly divided into fasting control group, gavage 50% glucose (2 g / kg) for 30, 60, 120 and 180 min groups. The tail vein glucose test results were observed at different time points. The changes of PGC-1α positive cells in the ventromedial hypothalamus of mice were semi-quantitatively detected by immunohistochemistry. Results Sugar load results: Compared with the fasting control group, the blood sugar began to increase after the glucose load, the highest blood glucose level was found in the 30 min group, and then decreased. The blood glucose level decreased to the pre-glucose level in 180 min group. They were 7.25 ± 2.84 (control group), 16.22 ± 3.51 (30 min group), 14.08 ± 4.14 (60 min group), 12.07 ± 1.85 (120 min group) and 10.12 ± 1.31 mmol / L (180 min group) respectively. Immunohistochemical results: Compared with the fasting control group, the number of PGC-1α positive neurons in the ventral medial nucleus of each group decreased significantly (P <0.05), and the lowest 120 min after the glucose load began to recover. Correlation analysis showed that there was a significant correlation between blood glucose level and the number of PGC-1α positive neurons in ventromedial hypothalamus (r = 0.983). Conclusions There is a significant correlation between the elevation of blood glucose and the down-regulation of PGC-1 expression in hypothalamic ventromedial neurons during the process of sugar loading in mice, suggesting that the hypothalamic PGC-1 expression may be one of the links in maintaining the stability of blood glucose.