McEvoy R C, Hegre O D
Diabetes. 1977 Dec;26(12):1140-6. doi: 10.2337/diab.26.12.1140.
The pancreatic insulin-, glucagon-, and somatostatin-positive cell populations were quantitated in normal and alloxan-diabetic rats. The method of quantitation (linear scanning) allowed an estimation of absolute changes in these cell populations through 14 months of diabetes. The changes in cell masses were correlated with changes in plasma and pancreatic immunoreactive insulin and glucagon. A marked reduction in the insulin-positive beta cells was demonstrated within seven days after alloxan treatment. No significant change in the glucagon-positive alpha cell population was noted in the diabetic rats when compared with normoglycemic controls. A statistically significant increase in the pancreatic somatostatin-positive delta cell population was demonstrable only after 14 months of alloxan diabetes. The results would suggest that the hyperglucagonemia of insulin-deficient diabetes is not a consequence of an increased pancreatic alpha cell population. In addition, since the increase in the pancreatic delta cell mass was found only late in the course of alloxan diabetes in the rat, the increase in delta cells is probably not of significance in the pathophysiology of diabetes in this experimental model.
对正常大鼠和四氧嘧啶糖尿病大鼠的胰腺胰岛素阳性、胰高血糖素阳性和生长抑素阳性细胞群进行了定量分析。定量方法（线性扫描）能够评估这些细胞群在长达14个月的糖尿病病程中的绝对变化。细胞质量的变化与血浆及胰腺中免疫反应性胰岛素和胰高血糖素的变化相关。四氧嘧啶处理后7天内，胰岛素阳性的β细胞显著减少。与血糖正常的对照组相比，糖尿病大鼠中胰高血糖素阳性的α细胞群未观察到显著变化。仅在四氧嘧啶糖尿病14个月后，胰腺生长抑素阳性的δ细胞群才有统计学意义的增加。结果表明，胰岛素缺乏型糖尿病的高胰高血糖素血症并非胰腺α细胞群增加的结果。此外，由于仅在大鼠四氧嘧啶糖尿病病程后期才发现胰腺δ细胞质量增加，在该实验模型中，δ细胞的增加可能在糖尿病病理生理学中并不重要。
