Lacombe C R, Viallard V P, Schaak S A, Paris H J
INSERM U 317, Institut Louis Bugnard, CHU Rangueil, Toulouse, France.
Diabetes Metab. 1996 Dec;22(6):432-8.
This study was undertaken to investigate the consequences of diabetes on Gi-protein expression and alpha 2-adrenergic receptivity in rat intestinal mucosa. Experimental diabetes was induced by treatment with streptozotocin. Quantification of alpha i-subunits by immunoblotting demonstrated that the level of the G alpha i2 but not the G alpha i3 subunit was markedly decreased in jejunum and colon membranes from diabetic rats as compared to controls. Parallel assessment of sympathetic innervation was performed by determination of norepinephrine content, measurement of tyrosine hydroxylase and monoamine oxidase activities, and quantification of alpha 2-adrenergic receptors in the different segments. At this stage of diabetes (6 weeks after streptozotocin injection), none of these parameters was significantly modified. Consequently, the decrease in G alpha i2 amount appears to be independent of the neuropathy describe in later stages of diabetes.
本研究旨在探讨糖尿病对大鼠肠黏膜Gi蛋白表达及α2-肾上腺素能受体敏感性的影响。通过链脲佐菌素处理诱导实验性糖尿病。免疫印迹法定量αi亚基表明，与对照组相比，糖尿病大鼠空肠和结肠膜中Gαi2亚基水平显著降低，而Gαi3亚基水平未降低。通过测定去甲肾上腺素含量、测量酪氨酸羟化酶和单胺氧化酶活性以及定量不同节段的α2-肾上腺素能受体，对交感神经支配进行了平行评估。在糖尿病的这个阶段（链脲佐菌素注射后6周），这些参数均未发生显著改变。因此，Gαi2数量的减少似乎与糖尿病后期描述的神经病变无关。
