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首页> 外文期刊>Cell and Tissue Research >The effect of glucagon-like peptide-1 in the management of diabetes mellitus: cellular and molecular mechanisms.
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The effect of glucagon-like peptide-1 in the management of diabetes mellitus: cellular and molecular mechanisms.

机译:胰高血糖素样肽1在糖尿病管理中的作用:细胞和分子机制。

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Incretins, such as glucagon-like peptide-1 (GLP)-1, have been shown to elevate plasma insulin concentration. The purpose of this study is to investigate the cellular and molecular basis of the beneficial effects of GLP-1. Normal and diabetic male Wistar rats were treated with GLP-1 (50 ng/kg body weight) for 10 weeks. At the end of the experiment, pancreatic tissues were taken for immunohistochemistry, immunoelectron microscopy and real-time polymerase chain reaction studies. Samples of blood were retrieved from the animals for the measurement of enzymes and insulin. The results show that treatment of diabetic rats with GLP-1 caused significant (P < 0.05) reduction in body weight gain and blood glucose level. GLP-1 (10(-12)-10(-6) M) induced significant (P < 0.01) dose-dependent increases in insulin release from the pancreas of normal and diabetic rats compared to basal. Diabetes-induced abnormal liver (aspartate aminotransferase and alanine aminotransferase) and kidney (blood urea nitrogen and uric acid) parameters were corrected in GLP-1-treated rats compared to controls. GLP-1 treatment induced significant (P < 0.05) elevation in the expression of pancreatic duodenal homeobox-1, heat shock protein-70, glutathione peroxidase, insulin receptor and GLP-1-receptor genes in diabetic animals compared to controls. GLP-1 is present in pancreatic beta cells and significantly (P < 0.05) increased the number of insulin-, glutathione reductase- and catalase-immunoreactive islet cells. The results of this study show that GLP-1 is co-localized with insulin and seems to exert its beneficial effects by increasing cellular concentrations of endogenous antioxidant genes and other genes involved in the maintenance of pancreatic beta cell structure and function.
机译:胰高血糖素样肽-1(GLP)-1等肠抑素可提高血浆胰岛素浓度。这项研究的目的是研究GLP-1有益作用的细胞和分子基础。正常和糖尿病雄性Wistar大鼠用GLP-1(50 ng / kg体重)治疗10周。实验结束时,取胰腺组织进行免疫组织化学,免疫电子显微镜和实时聚合酶链反应研究。从动物身上采集血样,以测量酶和胰岛素。结果表明,用GLP-1治疗糖尿病大鼠可显着(P <0.05)降低体重增加和血糖水平。与基础相比,GLP-1(10(-12)-10(-6)M)诱导正常和糖尿病大鼠胰腺中胰岛素释放的剂量依赖性显着增加(P <0.01)。与对照组相比,在用GLP-1处理的大鼠中,纠正了糖尿病引起的异常肝脏(天冬氨酸转氨酶和丙氨酸转氨酶)和肾脏(血尿素氮和尿酸)参数。与对照组相比,GLP-1处理在糖尿病动物中诱导胰腺十二指肠同源盒1,热休克蛋白70,谷胱甘肽过氧化物酶,胰岛素受体和GLP-1受体基因的表达显着(P <0.05)升高。 GLP-1存在于胰腺β细胞中,并且显着(P <0.05)增加了胰岛素,谷胱甘肽还原酶和过氧化氢酶免疫反应性胰岛细胞的数量。这项研究的结果表明,GLP-1与胰岛素共定位,并且似乎通过增加细胞内源性抗氧化剂基因和参与维持胰腺β细胞结构和功能的其他基因的浓度来发挥其有益作用。

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