吡格列酮对肝组织糖异生相关分子mRNA表达的影响

发布时间：2018-01-06 01:17

本文关键词：吡格列酮对肝组织糖异生相关分子mRNA表达的影响　出处：《军事医学》2016年05期 　论文类型：期刊论文

【摘要】：目的选用2型糖尿病自发性模型Goto-Kakisaki(GK)大鼠为实验对象,在观察靶向过氧化物酶体增生物激活受体γ(PPARγ)激动剂吡格列酮对糖尿病治疗作用的基础上,检测其对肝组织糖异生过程重要参与分子表达水平的影响。方法将GK大鼠随机分为3组:模型对照组、吡格列酮10、5 mg/kg组,另设Wistar大鼠为正常对照组。大鼠连续灌胃给药14 d,并在给药前、给药期间及给药后动态测定大鼠血糖、体质量变化;给药结束后次日进行糖耐量实验,逆转录聚合酶链反应(reverse transcriptase-polymerase chain reaction,RT-PCR)测定PPARγ、磷酸烯醇丙酮酸羧激酶(PEPCK)、葡糖-6-磷酸(G6P)、果糖-1,6-二磷酸酶(FBP1)、小异二聚体伙伴分子(SHP)mRNA表达。结果给药第14天血糖结果显示,与模型对照组血糖值(18.84±1.83)mmol/L相比,吡格列酮10、5 mg/kg剂量组大鼠血糖明显下降(P0.01),分别为(9.67±0.46)和(10.83±0.81)mmol/L;灌胃5%葡萄糖溶液120 min后,与模型组血糖值(11.4±1.0)mmol/L相比,吡格列酮10、5 mg/kg剂量组大鼠血糖明显下降(P0.01),分别为(6.0±0.9)和(5.7±0.6)mmol/L,糖耐量水平增强。给药14 d后,与模型组相比,吡格列酮10、5 mg/kg组大鼠肝组织中PPARγ、SHP的mRNA表达增加,PEPCK、G6P、FBP1的mRNA表达降低。结论该研究揭示了PPARγ激动剂的降糖效应,其途径之一是通过抑制糖异生得以实现,而且提示SHP很可能介入了PPARγ调控糖异生的过程。
[Abstract]:Objective to select the Goto-Kakisakiao GK rat model of type 2 diabetes mellitus as the experimental object. To observe the therapeutic effect of pioglitazone, a peroxisome proliferator-activated receptor (PPAR 纬) agonist, on diabetes mellitus. Methods GK rats were randomly divided into three groups: model control group, pioglitazone 105 mg/kg group. In addition, Wistar rats were used as normal control group. Rats were given intragastric administration for 14 days, and blood glucose and body mass were measured dynamically before, during and after administration. Glucose tolerance test was carried out the next day after administration. Reverse transcriptase polymerase chain reaction (RT-PCR) reverse transcriptase-polymerase chain reaction. PPAR 纬, phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphate (G6PN), fructose (-1) -6-diphosphatase (FBP1) were determined by RT-PCR. Results on the 14th day of administration, the results showed that the blood glucose level of the model control group was 18.84 卤1.83 渭 mol / L, compared with that of the model control group. In pioglitazone 10 ~ 5 mg/kg group, the blood glucose of rats decreased significantly (9.67 卤0.46) and 10.83 卤0.81 mmol / L, respectively. After 5% min of glucose solution, pioglitazone 10 was compared with the model group in blood glucose value of 11.4 卤1.0 mmol / L. 5 the blood glucose of rats in the mg/kg group decreased significantly (P 0.01) and 5.7 卤0.6 mmol / L, respectively. After 14 days of administration, compared with the model group, the mRNA expression of PPAR 纬 -SHP in the liver tissue of rats in pioglitazone 105 mg/kg group was increased compared with that in the model group. Conclusion this study revealed the hypoglycemic effect of PPAR 纬 agonist, which was achieved by inhibiting glycosylation. It is suggested that SHP may be involved in the regulation of glucose allogenesis by PPAR 纬.
【作者单位】：军事医学科学院放射与辐射医学研究所;南昌大学医学院;
【基金】：军事医学科学院创新基金(YC02016)
【分类号】：R587.1
【正文快照】： 糖尿病(diabetes mellitus,DM)严重危害人类健康,其中,2型糖尿病约占95%,主要表现为机体对胰岛素的抗性。近年来,该病在全球范围内呈上升趋势。靶向过氧化物酶体增生物激活受体γ(per-oxisome proliferators activated receptors,PPARγ)的噻唑烷二酮类(thiazolidinedione,TZD

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