Schmidt R E, Scharp D W
Diabetes. 1982 Sep;31(9):761-70. doi: 10.2337/diab.31.9.761.
Autonomic neuropathy involving the alimentary tract of several strains of inbred rats with chronic streptozotocin-induced diabetes has been characterized using ultrastructural methods. Markedly enlarged unmyelinated axons in the ileal mesentery of diabetic rats contain a variety of normal and unusual subcellular organelles similar to those described in experimental and clinical axonal dystrophies. These axonal alterations were seen after 6, 9, and 12 mo of diabetes, apparently increasing in frequency with time; lesions were absent, however, after only 3 1/2 mo of diabetes. An apparent proximo-distal gradient in the frequency of unmyelinated axonal lesions in this system suggests experimental diabetic autonomic neuropathy may represent an example of distal axonopathy. In addition, we have demonstrated an association of dystrophic axons with regenerative structures, including growth cones and clusters of filopodia.
利用超微结构方法对几种慢性链脲佐菌素诱导糖尿病的近交系大鼠消化道自主神经病变进行了特征描述。糖尿病大鼠回肠系膜中明显增粗的无髓轴突含有各种正常和异常的亚细胞器，类似于实验性和临床轴索性营养不良中所描述的那些。这些轴突改变在糖尿病6、9和12个月后可见，显然其发生率随时间增加；然而，糖尿病仅3个半月后则无病变。该系统中无髓轴突病变发生率明显的近-远梯度表明，实验性糖尿病自主神经病变可能是远端轴索性神经病的一个例子。此外，我们还证明了营养不良性轴突与再生结构（包括生长锥和丝状伪足簇）之间的关联。
