Bibi Yasmeen, Hussain Muhammad Mazhar, Naz Raeesa
J Ayub Med Coll Abbottabad. 2013 Jul-Dec;25(3-4):64-7.
Carnitine is an essential cofactor for the enzymes transporting long chain fatty acids across mitochondrial membranes for beta oxidation and also modulates the intra-mitochondrial acylCoA/CoA ratio. This study was conducted to determine the effect of levo-carnitine on endurance capacity, skeletal muscle fatigue characteristics and glycogen stores in diabetic rats.
This laboratory based experimental study was conducted in department of Physiology, Army Medical College, Rawalpindi, in collaboration with National Institute of Health (NIH), Islamabad, from June 2009 to July 2010. The study was carried on 60 healthy male Sprague-Dawley rats. Serum creatine phosphorkinase (CPK) levels were measured to exclude skeletal muscle disorder. Rats were fed high fat diet (2 weeks) followed by intra-peritoneal injection of streptozocin (35 mg/kg). On 21st day, after confirmation of type 2 diabetes by measuring plasma glucose and TG/HDL ratio, rats were divided into 2 equal groups; group I (Diabetic) and group II (Carnitine). Group II was administered 1-carnitine (200mg/kg) for 6 days. Both groups were further subdivided into 2 equal groups- a (swim group) and b (non-swim group). At end of 4th week, the rats of swim group were subjected to swimming test. The extensor digitorum muscle (EDL) of rats of non-swim group was dissected for evaluation of skeletal muscle fatigue characteristics. The glycogen content of EDL muscle and serum free carnitine (FC) levels of all groups were measured.
Carnitine treated rats exhibited improvement in swim time as well as skeletal muscle glycogen stores (p < 0.001). Significant improvement was also observed in skeletal muscle fatigue characteristics (p < 0.05). Serum free carnitine levels were also significantly raised in carnitine groups; the swim groups showed a lower FC levels as compared to their respective non-swim groups (p < 0.001).
Levocarnitine increases the glycogen stores and improves the skeletal muscle fatigue characteristics, leading to improvement in endurance capacity in type 2 diabetic rats.
肉碱是一种重要的辅助因子，可协助酶将长链脂肪酸转运穿过线粒体膜进行β氧化，还能调节线粒体内酰基辅酶A/辅酶A的比例。本研究旨在确定左旋肉碱对糖尿病大鼠耐力、骨骼肌疲劳特征和糖原储备的影响。
本基于实验室的实验研究于2009年6月至2010年7月在拉瓦尔品第陆军医学院生理学系与伊斯兰堡国家卫生研究所（NIH）合作开展。研究对象为60只健康雄性斯普拉格-道利大鼠。通过测量血清肌酸磷酸激酶（CPK）水平以排除骨骼肌疾病。大鼠先喂食高脂饮食2周，随后腹腔注射链脲佐菌素（35mg/kg）。在第21天，通过测量血糖和甘油三酯/高密度脂蛋白比值确认2型糖尿病后，将大鼠分为2个相等的组：I组（糖尿病组）和II组（肉碱组）。II组给予左旋肉碱（200mg/kg），持续6天。两组再进一步分为2个相等的组——a组（游泳组）和b组（非游泳组）。在第4周结束时，对游泳组的大鼠进行游泳测试。解剖非游泳组大鼠的趾长伸肌（EDL）以评估骨骼肌疲劳特征。测量所有组的EDL肌肉糖原含量和血清游离肉碱（FC）水平。
肉碱治疗的大鼠游泳时间以及骨骼肌糖原储备均有改善（p<0.001）。骨骼肌疲劳特征也有显著改善（p<0.05）。肉碱组的血清游离肉碱水平也显著升高；游泳组的FC水平低于各自的非游泳组（p<0.001）。
左旋肉碱增加糖原储备，改善骨骼肌疲劳特征，从而提高2型糖尿病大鼠的耐力。
