STZ誘発糖尿病ラットの外肛門括約筋の運動ニューロンと筋は糖尿病性神経障害に耐性がある

【Background/Aim】Functional decline in external anal sphincter (EAS) muscle might occur due to diabetic neuropathy (DN), which could result in various dysfunctions such as anal incontinence. Hyperglycemia has been reported to inhibit EAS function and decrease rectal compliance. However, there is no information on how diabetes affects EAS motoneurons and muscle. Therefore, we examined anatomical alterations in EAS motoneurons and muscle. 【Method】Type 1 diabetes was induced in 21 animals by administering streptozotocin (STZ). Twenty-two age-matched control animals were injected with saline. EAS motoneurons were retrogradely labeled using dextran-fluorescein, and the number and size of cell bodies were examined. EAS muscle fibers were stained using hematoxylin-eosin, and the myocyte sizes were determined. 【Results】No differences were observed in total number and size of EAS motoneurons, or diameter of EAS muscle fibers between the two groups. 【Discussion】The present study suggests that EAS motoneurons and their muscle are highly resistant to diabetes. However, it is unclear why these elements are resistant to diabetic changes. EAS motor nucleus consists only of alpha motoneurons, which are known to be highly resistant to diabetes among hindlimb motoneurons. Additionally, EAS muscle is in a state of constant weak contraction, except during defecation when relaxed and strongly contracted when cutting stool. This is unlike any other body part muscle. We considered that these characteristic activities, which differ from those of limb muscles, might contribute to maintenance of EAS motoneurons and their muscle. Future research to identify factors that affect tolerance to diabetes may reveal information that could be useful in preventing movement disorders caused by diabetes.