Increased Levels of Spinal Cord KIF1B Protein In Healthy and Diabetic Neuropathic Wistar Rats With in Adaptation to Aerobic Training (KIF1B Changes in Sensory Neurons After Exercise)

Abstract

Background and Objectives Diabetic neuropathy is one of the most common complications of diabetes and no suitable drug treatment has been found for this complication. The aim of this study was to determine the effect of six weeks of aerobic exercise on KIF1B protein in the sensory part of the spinal cord in rats with diabetic neuropathy. Subjects and Methods In the present experimental study, 12 male Wistar rats were divided into 4 groups: healthy exercise, control exercise, healthy diabetes and control diabetes. The training program included 6 weeks of running training on the treadmill in 5 sessions per week. The dorsal part of the spinal cord was analyzed as sensory neurons. Results The results showed that aerobic exercise significantly reduced blood glucose in the diabetic group compared to the control diabetes group (P=0.002), but no significant difference was observed in the weight of rats. The results also showed that a significant increase (P=0.044) in KIF1B in healthy exercise group compared to healthy control group and a significant increase (P=0.027) in KIF1B in diabetic exercise group compared to control diabetes. Conclusion The results showed that aerobic exercise increases the amount of KIF1B protein in healthy and diabetic rats, and this increase in KIF1B motor protein can improve axonal transmission and thus improve nerve function.

Axonal transport deficits in the pathogenesis of diabetic peripheral neuropathy

“…Exercise, as a non-drug pathway, exerts a beneficial effect in the treatment of DPN axonal transport defects. Endurance exercise inhibits the increase of KIF5, KIF1B, Dynein and other molecular motor protein contents in SCN of DPN rats ( 237 ), promotes axonal transport, and ameliorates nerve damage ( 238 , 239 ). Diabetic rats treated with gangliosides have been proven to prevent the progression of MNCV deficiency ( 240 – 243 ), and another study showed that gangliosides protect against impaired axonal transport of different molecular versions of acetylcholinesterase in diabetic animals ( 242 ).…”