ALLOXAN DIABETIC NEUROPATHY - ELECTRON-MICROSCOPIC STUDIES
ALLOXAN DIABETIC NEUROPATHY - ELECTRON-MICROSCOPIC STUDIES
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DOI：
10.1212/wnl.27.1.60
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发表时间：
1977-01-01
期刊：
影响因子：
9.9
通讯作者：
LAMPERT, P
中科院分区：
文献类型：
--
作者：
POWELL, H;KNOX, D;LAMPERT, P
对糖尿病大鼠注射四氧嘧啶后2年的周围神经进行了研究。观察到脱髓鞘和再脱髓鞘，轴突变性和再生，血管和雪旺细胞周围基层重复，增殖的雪旺细胞形成洋葱鳞茎。由纤维性电子致密物质聚集体组成的结晶沉积常发生在糖尿病动物的血管壁和神经内膜中，但很少见于年龄匹配的对照动物的神经中。糖原在线粒体内有髓鞘和无髓鞘轴突中积累。类似Lafora体的轴浆包涵体和IV型糖原病的包涵体是常见的，并且经常伴有颗粒糖原沉积。四氧嘧啶糖尿病的神经病变可能是由于轴突、雪旺氏细胞和血管的代谢损伤，导致节段性脱髓鞘和轴突变性。
Peripheral nerves of diabetic rats were studied 2 yr after alloxan injection. Demyelination and remyelination, axonal degeneration and regeneration, reduplication of basal laminae around vessels and Schwann''s cells and onion bulb formation by proliferated Schwann''s cells were observed. Crystalline deposits composed of aggregates of fibrillary electron dense material often occurred in vessel walls and endoneurium of diabetic animals but rarely were seen in nerves from age-matched control animals. Glycogen accumulated in myelinated and unmyelinated axons within mitochondria. Axoplasmic inclusions resembling Lafora''s bodies and the inclusions of glycogenosis type IV were frequent and often were accompanied by deposits of particulate glycogen. The neuropathy in alloxan diabetes may be caused by metabolic impairment of axons, Schwann''s cells and vessels, leading to segmental demyelination and axonal degeneration.