Abstract：
Currently, there are more than 10 million patients with diabetes mellitus in Japan. Therefore, the need to explore the pathogenesis of diabetes and the complications leading to its cure is becoming increasingly urgent. Pathological examination of pancreatic tissues from patients with type 2 diabetes reveals a decrease in the volume of beta cells because of a combination of various stresses. In human type 2 diabetes, islet amyloid deposition is a unique pathological change characterized by proinflammatory macrophage (M1) infiltration into the islets. The pathological changes in the pancreas with islet amyloid were different according to clinical factors, which suggests that type 2 diabetes can be further subclassified based on islet pathology. On the other hand, diabetic peripheral neuropathy is the most frequent diabetic complication. In early diabetic peripheral neuropathy, M1 infiltration in the sciatic nerve evokes oxidative stress or attenuates retrograde axonal transport, as clearly demonstrated by in vitro live imaging. Furthermore, islet parasympathetic nerve density and beta cell volume were inversely correlated in type 2 diabetic Goto-Kakizaki rats, suggesting that diabetic peripheral neuropathy itself may contribute to the decrease in beta cell volume. These findings suggest that the pathogenesis of diabetes mellitus and diabetic peripheral neuropathy may be interrelated.
摘要：
目前,日本有超过1000万糖尿病患者。因此,探讨糖尿病的发病机制及导致其治愈的并发症的必要性日益迫切。2型糖尿病患者胰腺组织的病理学检查显示，由于各种压力的组合，β细胞的体积减少。在人类2型糖尿病中，胰岛淀粉样蛋白沉积是一种独特的病理变化，其特征是促炎巨噬细胞（M1）浸润到胰岛中。胰岛淀粉样蛋白的病理改变因临床因素而异,这表明2型糖尿病可以根据胰岛病理学进一步细分。另一方面,糖尿病周围神经病变是最常见的糖尿病并发症。在早期糖尿病周围神经病变中，坐骨神经中的M1浸润引起氧化应激或减弱逆行轴突运输，如体外活体成像清楚地证明。此外，2型糖尿病Goto-Kakizaki大鼠胰岛副交感神经密度和β细胞体积呈负相关,提示糖尿病周围神经病变本身可能导致β细胞体积减少。这些发现表明糖尿病和糖尿病周围神经病变的发病机制可能是相互关联的。
