ACETYL-L-CARNITINE EFFECTS ON NERVE-CONDUCTION AND GLYCEMIC REGULATION IN EXPERIMENTAL DIABETES

Acetyl-L-Carnitine (ALC), an activator of carnitine, can accelerate ne rve regeneration after experimental surgical injury in rats. In this s tudy, we examined the ability of ALC to improve nerve conduction veloc ity and its effect on intravenous glucose tolerance test in streptozot ocin-induced diabetic rats. Diabetic (blood glucose > 200 mg%) and nor mal animals were treated intraperitoneally for four weeks with ALC, 50 mg/Kg/d and 150 mg/Kg/d. Nerve conduction velocity was measured by di rect exposure of sural nerve. Two-hour IVGTT was studied by measuring plasma glucose, insulin and free fatty acids after intravenous injecti on of glucose, 1.75 gm/Kg/body weight in animals treated either with A LC 150 mg/Kg/d or saline alone. Six weeks of STZ-induced diabetes resu lted in impairment of nerve conduction velocity in animals injected wi th saline (16.05 +/- 1.09 m/s), as compared to saline-treated normals who did not receive streptozotocin (31.9 +/- 0.84 m/s, p < 0.0005). Di abetic animals treated with ALC, 150 mg/Kg/d, preserved near normal ne rve 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 p lasma glucose in normal or diabetic rats, although it moderately reduc ed 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 < 0.00 3). Conclusion: ALC at a dose of 150 mg/Kg/d given for one month, prod uced near normalization of nerve conduction velocity in streptozotocin -induced diabetes with no adverse effects on glucose, insulin or free fatty acid levels.