本文關(guān)鍵詞：吡格列酮對(duì)肝組織糖異生相關(guān)分子mRNA表達(dá)的影響　出處：《軍事醫(yī)學(xué)》2016年05期 　論文類型：期刊論文

  更多相關(guān)文章： 吡格列酮 糖異生 PPARγ 糖尿病型 信使RNA

【摘要】：目的選用2型糖尿病自發(fā)性模型Goto-Kakisaki(GK)大鼠為實(shí)驗(yàn)對(duì)象,在觀察靶向過(guò)氧化物酶體增生物激活受體γ(PPARγ)激動(dòng)劑吡格列酮對(duì)糖尿病治療作用的基礎(chǔ)上,檢測(cè)其對(duì)肝組織糖異生過(guò)程重要參與分子表達(dá)水平的影響。方法將GK大鼠隨機(jī)分為3組:模型對(duì)照組、吡格列酮10、5 mg/kg組,另設(shè)Wistar大鼠為正常對(duì)照組。大鼠連續(xù)灌胃給藥14 d,并在給藥前、給藥期間及給藥后動(dòng)態(tài)測(cè)定大鼠血糖、體質(zhì)量變化;給藥結(jié)束后次日進(jìn)行糖耐量實(shí)驗(yàn),逆轉(zhuǎn)錄聚合酶鏈反應(yīng)(reverse transcriptase-polymerase chain reaction,RT-PCR)測(cè)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)、小異二聚體伙伴分子(SHP)mRNA表達(dá)。結(jié)果給藥第14天血糖結(jié)果顯示,與模型對(duì)照組血糖值(18.84±1.83)mmol/L相比,吡格列酮10、5 mg/kg劑量組大鼠血糖明顯下降(P0.01),分別為(9.67±0.46)和(10.83±0.81)mmol/L;灌胃5%葡萄糖溶液120 min后,與模型組血糖值(11.4±1.0)mmol/L相比,吡格列酮10、5 mg/kg劑量組大鼠血糖明顯下降(P0.01),分別為(6.0±0.9)和(5.7±0.6)mmol/L,糖耐量水平增強(qiáng)。給藥14 d后,與模型組相比,吡格列酮10、5 mg/kg組大鼠肝組織中PPARγ、SHP的mRNA表達(dá)增加,PEPCK、G6P、FBP1的mRNA表達(dá)降低。結(jié)論該研究揭示了PPARγ激動(dòng)劑的降糖效應(yīng),其途徑之一是通過(guò)抑制糖異生得以實(shí)現(xiàn),而且提示SHP很可能介入了PPARγ調(diào)控糖異生的過(guò)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 緯) 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 緯, 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 鹵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 鹵0.46) and 10.83 鹵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 鹵1.0 mmol / L. 5 the blood glucose of rats in the mg/kg group decreased significantly (P 0.01) and 5.7 鹵0.6 mmol / L, respectively. After 14 days of administration, compared with the model group, the mRNA expression of PPAR 緯 -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 緯 agonist, which was achieved by inhibiting glycosylation. It is suggested that SHP may be involved in the regulation of glucose allogenesis by PPAR 緯.
【作者單位】： 軍事醫(yī)學(xué)科學(xué)院放射與輻射醫(yī)學(xué)研究所;南昌大學(xué)醫(yī)學(xué)院;
【基金】：軍事醫(yī)學(xué)科學(xué)院創(chuàng)新基金(YC02016)
【分類號(hào)】：R587.1
【正文快照】： 糖尿病(diabetes mellitus,DM)嚴(yán)重危害人類健康,其中,2型糖尿病約占95%,主要表現(xiàn)為機(jī)體對(duì)胰島素的抗性。近年來(lái),該病在全球范圍內(nèi)呈上升趨勢(shì)。靶向過(guò)氧化物酶體增生物激活受體γ(per-oxisome proliferators activated receptors,PPARγ)的噻唑烷二酮類(thiazolidinedione,TZD

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本文編號(hào)：1385680