El-Salhy M, Spångéus A
Department of Medicine, University Hospital, Umeå, Sweden.
Dig Dis Sci. 1998 May;43(5):1031-7. doi: 10.1023/a:1018882818624.
The antral endocrine cells were investigated in nonobese diabetic (NOD) mice by means of immunohistochemistry, image analysis, and radioimmunoassays (RIA). As controls BALB/CJ mice of the same age and sex as the NOD mice were used. The number of gastrin- and somatostatin-immunoreactive cells was significantly decreased in both prediabetic and diabetic mice. There was no statistical difference between the NOD mice and controls regarding the serotonin-immunoreactive cells. Somatostatin levels as revealed by RIA in the antrum of both prediabetic and diabetic NOD mice were lower than those of the controls. There was no statistical difference in the level of antral gastrin between NOD mice and the controls. It was concluded that the changes in antral cells are primary to the onset of diabetes, and that the abnormalities observed in the antral cells in an animal model for diabetes type I might have relevance for the upper gastrointestinal dysfunction displayed in human diabetes.
通过免疫组织化学、图像分析和放射免疫测定法(RIA)对非肥胖糖尿病(NOD)小鼠的胃窦内分泌细胞进行了研究。作为对照,使用了与NOD小鼠年龄和性别相同的BALB/CJ小鼠。在糖尿病前期和糖尿病小鼠中,胃泌素和生长抑素免疫反应性细胞的数量均显著减少。NOD小鼠和对照之间血清素免疫反应性细胞没有统计学差异。糖尿病前期和糖尿病NOD小鼠胃窦中RIA显示的生长抑素水平低于对照。NOD小鼠和对照之间胃窦胃泌素水平没有统计学差异。得出的结论是,胃窦细胞的变化是糖尿病发病的原发性因素,并且在I型糖尿病动物模型中观察到的胃窦细胞异常可能与人类糖尿病中出现的上消化道功能障碍有关。