O'Brien T D, Hayden D W, Johnson K H, Fletcher T F
J Comp Pathol. 1986 Jul;96(4):357-69. doi: 10.1016/0021-9975(86)90031-9.
The anatomical distribution and volume fractions of pancreatic A cells (glucagon), B cells (insulin) and D cells (somatostatin) were evaluated by an immunoperoxidase technique in 6 diabetic cats, 6 normoglycaemic glucose-intolerant cats and 6 normal control cats. Islets lacking A cells were observed in some sections from the right lobe of the pancreas which correlated with a significantly lower A cell volume fraction in the right pancreatic lobe. Endocrine cell volume fractions in normoglycaemic glucose-intolerant cats were not significantly different from controls. Thus, a reduction in B cell volume fraction was not necessary for the occurrence of impaired glucose tolerance in these cats. However, the reduction of B cell volume fraction in the 2 normoglycaemic glucose-intolerant cats with insular amyloidosis may in part explain the more severely impaired glucose tolerance previously observed in these cats. Insular amyloidosis in our feline diabetics, as in human type II diabetics, was associated with a significant decrease in A and B cell volume fractions. In both human type II and feline diabetes mellitus, however, the reduction in B cell mass does not appear sufficient alone to lead to diabetes mellitus. Therefore, amyloid replacement of functional endocrine cells does not appear to be the primary diabetogenic event in feline diabetes mellitus, but may contribute to progression of the condition due to loss of functional B cell reserves. We thus postulate that a B cell defect precedes deposition of islet amyloid and that these amyloid deposits may thus provide an important biochemical clue to specific B cell derangements occurring in adult-onset diabetics.
采用免疫过氧化物酶技术，对6只糖尿病猫、6只血糖正常但糖耐量异常的猫和6只正常对照猫的胰腺A细胞（胰高血糖素）、B细胞（胰岛素）和D细胞（生长抑素）的解剖分布及体积分数进行了评估。在胰腺右叶的一些切片中观察到缺乏A细胞的胰岛，这与右胰腺叶中A细胞体积分数显著降低相关。血糖正常但糖耐量异常的猫的内分泌细胞体积分数与对照组无显著差异。因此，在这些猫中，糖耐量受损的发生并不一定需要B细胞体积分数降低。然而，2只患有胰岛淀粉样变的血糖正常但糖耐量异常的猫的B细胞体积分数降低，可能部分解释了之前在这些猫中观察到的更严重的糖耐量受损情况。与人类II型糖尿病患者一样，我们的猫糖尿病患者的胰岛淀粉样变与A细胞和B细胞体积分数显著降低有关。然而，在人类II型糖尿病和猫糖尿病中，B细胞质量的降低似乎单独并不足以导致糖尿病。因此，功能性内分泌细胞的淀粉样替代似乎不是猫糖尿病的主要致糖尿病事件，但可能由于功能性B细胞储备的丧失而导致病情进展。因此，我们推测B细胞缺陷先于胰岛淀粉样变的沉积，因此这些淀粉样沉积物可能为成年发病糖尿病患者中发生的特定B细胞紊乱提供重要的生化线索。
