Soneru I L, Khan T, Orfalian Z, Abraira C
Extended Care & Geriatrics Service (181C), Hines VA Hospital, Illinois 60141, USA.
Endocr Res. 1997 Feb-May;23(1-2):27-36. doi: 10.1080/07435809709031840.
Acetyl-L-Carnitine (ALC), an activator of carnitine, can accelerate nerve regeneration after experimental surgical injury in rats. In this study, we examined the ability of ALC to improve nerve conduction velocity and its effect on intravenous glucose tolerance test in streptozotocin-induced diabetic rats. Diabetic (blood glucose > 200 mg%) and normal animals were treated intraperitoneally for four weeks with ALC, 50 mg/Kg/d and 150 mg/Kg/d. Nerve conduction velocity was measured by direct exposure of sural nerve. Two-hour IVGTT was studied by measuring plasma glucose, insulin and free fatty acids after intravenous injection of glucose, 1.75 gm/Kg/body weight in animals treated either with ALC 150 md/Kg/d or saline alone. Six weeks of STZ-induced diabetes resulted in impairment of nerve conduction velocity in animals injected with saline (16.05 +/- 1.09 m/s), as compared to saline-treated normals who did not receive streptozotocin (31.0 +/- 0.84 m/s, p<0.0005). Diabetic animals treated with ALC, 150 mg/Kg/d, preserved near normal nerve conduction (27.10 +/- 1.42 m/s), compared with the saline-treated diabetic animals (p < 0.0005), but diabetic animals treated with ALC, 50 mg/Kg/d, had a non-significant increase in nerve conduction (23.68 +/- 1.6). ALC treatment had no effect on fasting or post-intravenous plasma glucose in normal or diabetic rats, although it moderately reduced baseline and 40 minute insulin levels (p < 0.02) in normal rats as compared with their saline-treated counterparts. ALC treatment lowered baseline free fatty acids in normal (p < 0.04) and diabetic (p < 0.03) animals, and the 60 minute levels in the normal group only (p < 0.003).
ALC at a dose of 150 mg/Kg/d given for one month, produced near normalization of nerve conduction velocity in streptozotocin-induced diabetes with no adverse effects on glucose, insulin or free fatty acid levels.
乙酰左旋肉碱（ALC）是肉碱的一种激活剂，可加速大鼠实验性手术损伤后的神经再生。在本研究中，我们检测了ALC改善链脲佐菌素诱导的糖尿病大鼠神经传导速度的能力及其对静脉葡萄糖耐量试验的影响。糖尿病（血糖>200mg%）和正常动物腹腔注射ALC，剂量分别为50mg/Kg/d和150mg/Kg/d，持续四周。通过直接暴露腓肠神经来测量神经传导速度。在静脉注射葡萄糖（1.75gm/Kg/体重）后，通过测量血浆葡萄糖、胰岛素和游离脂肪酸来研究两小时的静脉葡萄糖耐量试验，受试动物分别为接受150mg/Kg/d ALC治疗或仅接受生理盐水治疗的动物。与未接受链脲佐菌素治疗的生理盐水处理的正常动物（31.0±0.84m/s，p<0.0005）相比，六周的链脲佐菌素诱导的糖尿病导致注射生理盐水的动物神经传导速度受损（16.05±1.09m/s）。与生理盐水处理的糖尿病动物相比，接受150mg/Kg/d ALC治疗的糖尿病动物神经传导接近正常（27.10±1.42m/s，p<0.0005），但接受50mg/Kg/d ALC治疗的糖尿病动物神经传导增加不显著（23.68±1.6）。ALC治疗对正常或糖尿病大鼠的空腹或静脉注射后血浆葡萄糖无影响，尽管与生理盐水处理的正常大鼠相比，它适度降低了正常大鼠的基线和40分钟胰岛素水平（p<0.02）。ALC治疗降低了正常（p<0.04）和糖尿病（p<0.03）动物的基线游离脂肪酸水平，且仅降低了正常组60分钟时的游离脂肪酸水平（p<0.003）。
以150mg/Kg/d剂量给予ALC一个月，可使链脲佐菌素诱导的糖尿病大鼠神经传导速度接近正常，且对葡萄糖、胰岛素或游离脂肪酸水平无不良影响。
