Efrat S, Fleischer N, Hanahan D
Cold Spring Harbor Laboratory, New York 11724.
Mol Cell Biol. 1990 Apr;10(4):1779-83. doi: 10.1128/mcb.10.4.1779-1783.1990.
Transgenic mice expressing an insulin-promoted H-ras hybrid gene in pancreatic beta cells developed beta-cell degeneration and diabetes. The disease was manifested in male mice by hyperglycemia, glycosuria, and reduced plasma insulin levels, which appeared around 5 months of age and led to premature death. Histological analyses revealed large holes within the islets of Langerhans and a reduced number of beta cells. The destruction of the islets was not associated with an obvious inflammatory activity. Ultrastructural analysis showed extensive engorgement in the endoplasmic reticulum of the residual beta cells from diabetic males. The females carrying the insulin-promoted ras gene did not manifest any of the physiological abnormalities observed in males and showed only minor histological and ultrastructural changes, even at much greater ages.
在胰腺β细胞中表达胰岛素促进型H-ras杂交基因的转基因小鼠发生了β细胞变性和糖尿病。这种疾病在雄性小鼠中表现为高血糖、糖尿和血浆胰岛素水平降低，这些症状在大约5个月大时出现，并导致过早死亡。组织学分析显示，胰岛内有大洞，β细胞数量减少。胰岛的破坏与明显的炎症活动无关。超微结构分析显示，糖尿病雄性小鼠残留β细胞的内质网广泛扩张。携带胰岛素促进型ras基因的雌性小鼠没有表现出雄性小鼠中观察到的任何生理异常，即使在年龄大得多的时候，也只表现出轻微的组织学和超微结构变化。
