Does Endurance Training Compensate for Neurotrophin Deficiency Following Diabetic Neuropathy?

نویسندگان

1 Faculty of Physical Education and Sport Sciences, Allameh Tabataba’i University, Tehran, IR Iran

2 Physical Education Department, Faculty of Humanity and Literature, Tarbiat Modares University, Tehran, IR Iran

3 Physical Education Department, Faculty of Humanity and Literature, Vali-e-Asr University of Rafsanjan, Rafsanjan, IR Iran

4 Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, IR Iran

5 Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, IR Iran

doi
چکیده

A lack of neurotrophic support is believed to contribute to the development of diabetic neuropathy. On the otherhand, neurotrophins have consistently been shown to increase in the central and peripheral nervous system following exercise, butthe effects of exercise intervention on brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in diabetic neuropathyare not understood.Objectives: This experimental study was designed and carried out at the Tarbiat Modares university (TMU) in Tehran, Iran, to investigatethe hypothesis that increased activity as endurance training can help to increase the endogenous expression of neurotrophinsin diabetic rats.Methods: This was an experimental study with 22 factorial plans performed atTMUin Iran. Sampling was accidental and 28 adultmale Wistar rats in the body mass range of 326.3  8.4 g comprised the sample, with each rat randomly assigned to four groups:diabetic control (DC), diabetic training (DT), healthy control (HC), and healthy training (HT). To induce diabetic neuropathy, after12 hours of food deprivation, an intraperitoneal injection of streptozotocin (STZ) solution (45 mg/Kg) method was used. Two weeksafter STZ injection, the endurance training protocol was performed for 6 weeks; 24 hours after the last training session, the rats weresacrificed. Real-time PCR was used for BDNF and NGF expression.Results: The data indicate that diabetes decreasesBDNFandNGFexpression in sensory (92%, P=0.01; 90%, P=0.038, respectively)andmotor (93%, P = 0.05; 60%, P = 0.029, respectively) roots. However, NGF mRNA levels in the DT group were significantly higher thanin the HC group ((7.1-fold), P = 0.01; (2.2-fold), P = 0.001, respectively, for sensory and motor roots), but this was not shown for BDNF.In addition, endurance training can increase NGF expression in healthy rats ((7.4-fold), P = 0.01; (3.8-fold), P = 0.001, respectively, forsensory and motor roots).Conclusions: This study shows that BDNF and NGF expression decreases in diabetic neuropathy. However, this decrease can bereversed through endurance training. These results also indicate that endurance trainingmayhave a potential role in compensatingfor neurotrophin deficiency following diabetic neuropathy.