Effects of acetyl- and proprionyl- l-carnitine on peripheral nerve function and vascular supply in experimental diabetes

l-Carnitine metabolism is abnormal in diabetes mellitus, and treatment with acetyl- l-carnitine (ALC) improves the function of cardiac muscle, retina, and peripheral nerve in experimental models. The aim was to compare the effects of ALC and proprionyl- l-carnitine (PLC) on motor and sensory nerve conduction in streptozotocin-diabetic rats and to ascertain whether their action could be mediated by a vascular mechanism. ALC and PLC treatment for 2 months after diabetes induction attenuated the development of sciatic motor nerve conduction velocity (NCV) deficits by 59.4% ± 4.4% and 46.9% ± 3.2%, respectively. There was a similar level of protection for sensory saphenous NCV (42.9% ± 6.6% and 47.8% ± 6.0%, respectively). Neither ALC nor PLC prevented the development of resistance to hypoxic conduction failure (RHCF) in sciatic nerve from diabetic rats. A 46.5% ± 3.4% deficit in sciatic endoneurial blood flow, measured by microelectrode polarography and hydrogen clearance, in diabetic rats was partially prevented by both ALC (48.7% ± 6.4%) and PLC (69.4% ± 10.1%). ALC had no significant effect on blood flow in nondiabetic rats. Thus, the data show that these l-carnitine derivatives have a similar efficacy in preventing nerve dysfunction, which depends on a neurovascular action.