Petersen K G, Heilmeyer P, Kerp L
Diabetologia. 1975 Feb;11(1):21-5. doi: 10.1007/BF00422813.
The protein synthesis in normal and in EMC-virus infected mouse islets of Langerhans was investigated. Mouse large glucagon immunoreactivity was determined by an immunoassay after chromatographic separation. It was characterized as a peptide of 16 000 MW with in intracellular half-life of 35-45 min. The proportional reduction of void volume proteins, large glucagon immunoreactivity and proinsulin synthesis after infection shows, that both alpha- and beta-cells are damaged by the virus. A reduction in the synthesis of the three protein fractions was already found 6 hrs after inoculation of the virus and remained nearly constant for 48 hrs. An almost complete breakdown of protein synthesis occurred 60 to 70 hrs after infection and was paralleled by the first light microscopic changes in the islets. The stimulation of proinsulin synthesis by glucose was preserved for 48 hrs after EMC-virus infection.
对正常和感染脑心肌炎病毒(EMC-virus)的小鼠胰岛中的蛋白质合成进行了研究。通过色谱分离后的免疫测定法测定小鼠大胰高血糖素免疫反应性。其被表征为分子量为16000的肽,细胞内半衰期为35 - 45分钟。感染后空体积蛋白、大胰高血糖素免疫反应性和胰岛素原合成的比例性降低表明,α细胞和β细胞均受到病毒损害。在接种病毒6小时后就已发现这三种蛋白质组分的合成减少,并在48小时内几乎保持恒定。感染后60至70小时发生了几乎完全的蛋白质合成崩溃,同时胰岛出现了最初的光学显微镜变化。在EMC病毒感染后,葡萄糖对胰岛素原合成的刺激作用持续了48小时。