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Background: Diabetic peripheral neuropathy (DPN) is a typical complication of diabetes. No definitive treatment and prevention of DPN has been established, and very few data on the role of exercise training on DPN have been reported., Aim of the Study: The protective and therapeutic effects of aerobic physical activity on the development of DPN in Type 1 were investigated., Methods: Rats were assigned to 5 groups: C (control), E (exercise), D (diabetic), DEx (exercise after diabetic), ExD (diabetic after exercise); C containing 10 animals and E, D, DEx, ExD containing 15 animals. Diabetes was induced with streptozotocin (STZ) (45 mg/kg, ip). Development of diabetes was confirmed by measuring blood glucose levels 2 days after STZ treatment. Body weights of all the animals were evaluated weekly throughout the experiment. Motor dysfunction defined by a significant increase in compound muscle action potential (CMAP) latency was recorded. The amplitude of CMAP which mainly reflects axonal dysfunction was also measured using standard techniques. Sciatic nerve morphometry and blood glucose levels were analyzed in all the groups., Results: Blood glucose level significantly increased 2 days after STZ injection. All diabetic rats showed decreased body weight compared to control rats. An increase in motor latency of CMAP and a decrease in amplitude of CMAP, indicative of neuropathy, were seen in STZ rats. On the completion of the study (the 56th day post-STZ), histological examination revealed significant myelin loss (thinner myelin) in sciatic nerves of STZ rats. Treatment with swimming exercise had no effect on glycemic control but restored body weight, CMAP amplitude, CMAP latency or motor dysfunction in the diabetic animals., Conclusions: This study suggests that swimming exercise training has protective and therapeutic effects on DPN of STZ-induced diabetic rats.

Erythropoietin (EPO) possesses generalized neuroprotective and neurotrophic actions. We tested the efficacy of recombinant human EPO (rhEPO) in preventing and reversing nerve dysfunction in streptozotocin (STZ)-induced diabetes in rats. Two days after STZ [60 mg/kg of body weight (b.w.), i.p.], diabetic animals were administered rhEPO (40 microg/kg of b.w.) three times weekly for 5 weeks either immediately (preventive) before or after a 5-week delay (therapeutic) after induction of hyperglycemia or at a lower dose (8 microg/kg of b.w. once per week) for 8 weeks (prolonged). Tail-nerve conduction velocities (NCV) was assessed at 5 and 11 weeks for the preventive and therapeutic schedule, respectively. Compared to nondiabetic rats, NCV was 20% lower after 5 weeks in the STZ group, and this decrease was attenuated 50% by rhEPO. Furthermore, the reduction of Na(+),K(+)-ATPase activity of diabetic nerves (by 55%) was limited to 24% in the rhEPO-treated group. In the therapeutic schedule, NCV was reduced by 50% after 11 weeks but by only 23% in the rhEPO-treated group. rhEPO treatment attenuated the decrease in compound muscle action potential in diabetic rats. In addition, rhEPO treatment was associated with a preservation of footpad cutaneous innervation, as assessed by protein gene product 9.5 immunostaining. Diabetic rats developed alterations in mechanical and thermal nociception, which were partially reversed by rhEPO given either in a preventative or therapeutic manner. These observations suggest that administration of rhEPO or its analogues may be useful in the treatment of diabetic neuropathy.