發(fā)布時(shí)間：2018-02-05 00:52

  本文關(guān)鍵詞： 胰島素抵抗 胰島素受體 一氧化氮 誘導(dǎo)型-氧化氮合酶 氨基胍　出處：《山東大學(xué)》2005年碩士論文　論文類型：學(xué)位論文

【摘要】：目的:以外周血白細(xì)胞作為靶細(xì)胞,檢測(cè)高糖飲食誘導(dǎo)的胰島素抵抗大鼠及加用氨基胍治療大鼠胰島素信號(hào)轉(zhuǎn)導(dǎo)通路關(guān)鍵分子mRNA及誘導(dǎo)型一氧化氮合酶mRNA(iNOS mRNA)的表達(dá),并通過(guò)血生化指標(biāo)的檢測(cè),從基因轉(zhuǎn)錄水平上探討胰島素抵抗的發(fā)病機(jī)制和氨基胍的保護(hù)作用機(jī)制。 方法:將Wistar大鼠隨機(jī)分為正常對(duì)照組、高糖對(duì)照組以及高糖加氨基胍(AG)治療組,飼養(yǎng)6個(gè)月,每月斷尾取血,用本室設(shè)計(jì)的優(yōu)化原位雜交技術(shù)測(cè)定外周血白細(xì)胞iNOS mRNA、胰島素受體mRNA(IR mRNA)、磷脂酰肌醇3-激酶P85 α亞單位mRNA(PI-3K P85 α亞單位mRNA)、蛋白激酶B α mRNA(PKB α mRNA)、蛋白激酶B β mRNA(PKB β mRNA)及葡萄糖轉(zhuǎn)運(yùn)蛋白2mRNA(GLUT2 mRNA)的表達(dá)情況。每月測(cè)定空腹血漿血糖、胰島素、糖化血清蛋白(GSP)及一氧化氮(NO)含量。比較各組血生化指標(biāo)、外周血白細(xì)胞iNOS mRNA以及胰島素信號(hào)轉(zhuǎn)導(dǎo)通路分子mRNA表達(dá)水平的差異。 結(jié)果:高糖對(duì)照組血糖、血漿胰島素、GSP及NO水平高于正常對(duì)照組,胰島素敏感指數(shù)低于正常對(duì)照組;外周血白細(xì)胞iNOS mRNA和PKB α mRNA表達(dá)水平高于正常對(duì)照組,IR mRNA、PI-3K P85 α亞單位mRNA、PKB β mRNA表達(dá)水平低于正常對(duì)照組,GLUT2 mRNA表達(dá)水平無(wú)變化。 AG治療組血生化指標(biāo)及外周血白細(xì)胞信號(hào)分子mRNA的表達(dá)與高糖對(duì)照組具有相同的變化趨勢(shì)。但隨著AG治療時(shí)間的延長(zhǎng),與高糖對(duì)照組相比,2月后,血漿NO水平降低,外周血白細(xì)胞IR mRNA表達(dá)水平升高;5月后,血糖、血漿GSP較高糖對(duì)照組降低,外周血白細(xì)胞iNOS mRNA,PKB α mRNA表達(dá)水平降低,且后者恢復(fù)至正常水平,PI-3K P85 α亞單位mRNA、PKB β mRNA表達(dá)水平升高,且前者于6月時(shí)恢復(fù)至正常水平,胰島素敏感指數(shù)于6月時(shí)升高;兩組各月血漿胰島素水平與外周血白細(xì)胞GLUT2 mRNA表達(dá)水平無(wú)顯著差異。
[Abstract]:Objective: to use peripheral white blood cells as target cells. The insulin resistance rats induced by high glucose diet and the rats treated with aminoguanidine were detected. The key molecules of insulin signal transduction pathway (mRNA) and inducible nitric oxide synthase (mRNA(iNOS) mRNAs were detected. The expression of. The pathogenesis of insulin resistance and the protective mechanism of aminoguanidine were discussed from the level of gene transcription. Methods: Wistar rats were randomly divided into normal control group, high glucose control group and high sugar plus aminoguanidine group. The iNOS mRNAs and insulin receptor mRNA(IR mRNAs in peripheral blood leukocytes were determined by the optimized in situ hybridization technique designed by our laboratory. Phosphatidylinositol 3-kinase P85 偽 subunit mRNA(PI-3K P85 偽 subunit mRNAs, protein kinase B 偽 mRNA(PKB 偽 mRNAs. The expression of protein kinase B 尾 mRNA(PKB 尾 mRNAand glucose transporter 2mRNA-GLUT2 mRNA. fasting plasma glucose and insulin were measured monthly. The contents of glycosylated serum protein (GSPs) and nitric oxide (no) were compared in each group. The expression levels of iNOS mRNA and insulin signal transduction pathway (mRNA) in peripheral blood leukocytes were different. Results: the levels of blood glucose, plasma insulin GSP and no in the hyperglycemic control group were higher than those in the normal control group, and the insulin sensitivity index was lower than that in the normal control group. The expression levels of iNOS mRNA and PKB 偽 mRNA in peripheral blood leukocytes were higher than those in control group. The expression of PI-3K P85 偽 subunit mRNA was higher than that of normal controls. The expression level of PKB 尾 mRNA was lower than that of control group. There was no change in GLUT2 mRNA expression. The changes of serum biochemical indexes and the expression of mRNA in peripheral blood leukocytes in AG treatment group were similar to those in high glucose control group, but with the prolongation of AG treatment time, it was compared with high glucose control group. After February, the level of plasma no decreased and the expression of IR mRNA in peripheral blood leukocytes increased. After May, blood glucose and plasma GSP were lower than those of high glucose control group, and the expression of iNOS mRNA-PKB 偽 mRNA in peripheral white blood cells was decreased, and the latter returned to normal level. The expression of PI-3K P85 偽 subunit mRNA-PKB 尾 mRNA increased, and the former returned to normal level on June, and the insulin sensitivity index increased on June. There was no significant difference between the level of plasma insulin and the expression of GLUT2 mRNA in peripheral blood leukocytes between the two groups.
【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2005
【分類號(hào)】：R363

【共引文獻(xiàn)】

相關(guān)期刊論文 前10條

1 ;[J];;2002年04期

2 ;[J];;2002年04期

3 ;[J];;2002年04期

4 ;[J];;2002年04期

5 余峰彬;胰島素抵抗的分子機(jī)制[J];攀枝花學(xué)院學(xué)報(bào);2004年06期

6 張怡梅,劉斌,任朝英,李書君,賈漪濤,李慶霞;惡性腫瘤與胰島素抵抗[J];腫瘤防治雜志;2003年01期

7 狄靚亮;袁國(guó)躍;周麗斌;賈玨;王東;陳軍建;;羅格列酮對(duì)3T3-L1脂肪細(xì)胞chemerin表達(dá)的影響[J];山東醫(yī)藥;2011年12期

8 駱天紅;趙萸;李果;張宏利;李文毅;劉優(yōu)萍;羅敏;王侃侃;張濟(jì);鄭培p，

本文編號(hào)：1491644