Tamaki Toru, Muramatsu Ken, Ikutomo Masako, Oshiro Naomi, Hayashi Hisae, Niwa Masatoshi
Department of Occupational Therapy, Graduate School of Kyorin University, 5-4-1 Simorenzyaku, Mitaka-city, Tokyo, 181-8612, Japan.
Department of Physical Therapy, Health Science University, 7187 Kodachi, Fujikawaguchiko-town, Yamanashi, 401-0380, Japan.
Anat Sci Int. 2018 Sep;93(4):502-513. doi: 10.1007/s12565-018-0444-z. Epub 2018 Jun 6.
Skeletal muscle fiber subtypes are differentially sensitive to diabetes-related pathology; For example, fast-twitch muscles exhibit severe decreases in contraction force while slow-twitch muscles demonstrate prolonged half-relaxation time. However, such alterations have only been examined after a relatively short period following diabetes onset, with no information available regarding muscle damage caused by longer disease periods (>20 weeks). This study examined alterations in the contractile properties of the medial gastrocnemius (fast-twitch) and soleus (slow-twitch) muscles, as well as morphological changes in their motor neurons 12 and 22 weeks after diabetes onset. Adult male Wistar rats were divided into diabetic (12- or 22-week post-streptozotocin injection) and age-matched control groups. Electrically evoked maximum twitch and tetanic tension were recorded from leg muscles. Additionally, motor neuron number and cell body size were examined. At 12 weeks after diabetes onset, decreases in twitch force were observed predominantly in medial gastrocnemius muscles, while soleus muscles exhibited prolonged half-relaxation time. However, these differences became ambiguous at 22 weeks, with decreased twitch force and prolonged half-relaxation time observed in both muscles. On the other hand, reduction in soleus motor neurons was observed 12 weeks after diabetes onset, while medial gastrocnemius motor neurons were diminished at 22 weeks. These data indicate that experimental diabetes induces differential damage to medial gastrocnemius and soleus muscles as well as motor neurons. These diabetes-induced differences may partly underlie the differential deficits observed in gastrocnemius and soleus.
骨骼肌纤维亚型对糖尿病相关病理变化的敏感性存在差异；例如，快肌在收缩力方面表现出严重下降，而慢肌则显示半松弛时间延长。然而，此类变化仅在糖尿病发病后的相对短时间内进行了研究，关于较长病程（>20周）所导致的肌肉损伤尚无相关信息。本研究检测了糖尿病发病12周和22周后，腓肠肌内侧（快肌）和比目鱼肌（慢肌）收缩特性的改变，以及其运动神经元的形态变化。成年雄性Wistar大鼠被分为糖尿病组（链脲佐菌素注射后12周或22周）和年龄匹配的对照组。记录腿部肌肉的电诱发最大抽搐和强直张力。此外，检测运动神经元数量和细胞体大小。糖尿病发病12周时，主要在腓肠肌内侧观察到抽搐力下降，而比目鱼肌则表现出半松弛时间延长。然而，在22周时这些差异变得不明显，两块肌肉均出现抽搐力下降和半松弛时间延长。另一方面，糖尿病发病12周后观察到比目鱼肌运动神经元减少，而腓肠肌内侧运动神经元在22周时减少。这些数据表明，实验性糖尿病会对比目鱼肌和腓肠肌以及运动神经元造成不同程度的损伤。这些糖尿病诱导的差异可能部分解释了腓肠肌和比目鱼肌中观察到的不同缺陷。
