Klueber K M, Feczko J D
Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Kentucky 40292.
Anat Rec. 1994 May;239(1):18-34. doi: 10.1002/ar.1092390104.
Since peripheral nerves are damaged in diabetes mellitus, morphological changes occur within the diabetic muscle in response to the diabetic neuropathy. The aim of this study was to examine the extensor digitorum longus (EDL) from a 42-day streptozotocin-induced diabetic Swiss Webster mouse (STZ) and compare the muscle morphology and histochemistry to age-matched, nondiabetic controls.
The EDL was evaluated using electron microscopy in order to investigate the morphological integrity of the myofibers and neuromuscular junctions. Histochemical analysis was completed using the myofibrillar CA(++)-ATPase reaction of Doriguzzi et al. (1983. Histochemistry, 79:289-294) for use in computer-assisted morphometric analysis of fiber size using Bioquant System 4 software.
Ultrastructural analysis of the diabetic EDL (N = 5, 225 myofibers/animal) showed a significant number of abnormal myofibers, exhibiting various degrees of degeneration, signs of denervation, and necrosis. The STZ myofibers exhibited excessive lipid accumulations and abnormal mitochondrial arrangements. Histochemical analysis of the STZ EDL revealed a significant shift in fiber type profile (53.6% type 2A and 46.4% type 2B- STZ myofibers; 47.5% type 2A, 52.5% type 2B nondiabetic controls). Morphometric analysis of myofiber size by fiber type (200 myofibers/muscle/fiber type) indicated a significant decrease in myofiber size for both type 2A and type 2B fibers in the STZ diabetic mouse.
The degeneration and necrosis of myofibers concomitant with the sever atrophy of both the type 2A and 2B myofibers in the STZ muscle could account for the functional alterations seen in diabetic muscle.
由于糖尿病会导致周围神经损伤，糖尿病性肌肉会发生形态学变化以应对糖尿病性神经病变。本研究的目的是检查42天链脲佐菌素诱导的糖尿病瑞士韦伯斯特小鼠（STZ）的趾长伸肌（EDL），并将其肌肉形态和组织化学与年龄匹配的非糖尿病对照组进行比较。
使用电子显微镜评估EDL，以研究肌纤维和神经肌肉接头的形态完整性。组织化学分析采用多里古齐等人（1983年。组织化学，79:289 - 294）的肌原纤维CA(++) - ATP酶反应，并使用Bioquant System 4软件进行纤维大小的计算机辅助形态计量分析。
对糖尿病EDL（N = 5，每只动物225条肌纤维）的超微结构分析显示，大量异常肌纤维出现，表现出不同程度的变性、去神经支配迹象和坏死。STZ肌纤维表现出过多的脂质积累和异常线粒体排列。对STZ EDL进行组织化学分析发现，纤维类型分布有显著变化（STZ肌纤维中2A型占53.6%、2B型占46.4%；非糖尿病对照组中2A型占47.5%、2B型占52.5%）。按纤维类型对肌纤维大小进行形态计量分析（每种纤维类型每块肌肉200条肌纤维）表明，STZ糖尿病小鼠的2A型和2B型纤维的肌纤维大小均显著减小。
STZ肌肉中肌纤维的变性和坏死以及2A型和2B型肌纤维的严重萎缩可能是糖尿病肌肉功能改变的原因。
