Masoud Rahmati1, Reza Gharakhanlou2, Mansoureh Movahedin3, Seyed Javad Mowla4, Ali Khazani5, Maryam Fouladvand6, Shiva Jahani Golbar7. 1. Department of Physical Education and Sport Sciences, Faculty of Literature and Humanities, Lorestan University, Khorramābād, Iran. ghara_re@modares.ac.ir. 2. Department of Physical Education and Sport Sciences, Faculty of Humanities, Tarbiat Modares University, Tehran, Iran. 3. Department of Anatomical Sciences, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. 4. Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran. 5. Department of Physical Education and Sport Sciences, Faculty of Humanities, Islamic Azad University, Ardabil, Iran. 6. Young Researchers and Elite Club, Borujerd Branch, Islamic Azad University, Borujerd, Iran. 7. Department of Physical Education and Sport Sciences, Tehran Kish International University, Tehran, Iran.
Abstract
BACKGROUND: Previous research has demonstrated diabetic-induced axonal transport deficits. However, the mechanism of axonal transport impairment induced by diabetes is poorly understood. Kinesin motor proteins have been shown to transport various cargos along highly polarized neurons. In the present study, we investigated the effect of regular treadmill exercise on KIF5B and Sunday Driver (SYD) mRNA levels in sensory and motor parts of spinal cord and KIF5B content in sciatic nerves of streptozotocin (STZ)-induced diabetic rats. METHODS: Forty male Wistar rats were divided into four groups: (1) diabetic trained (DT: n = 10); (2) Non-trained diabetic (NTD: n = 10); (3) normal control (NC: n = 10), and (4) normal trained (NT: n = 10). Two weeks after STZ injection (45 mg/kg, i.p.), the rats were subjected to treadmill exercise for 5 days a week over 6 weeks. We determined mRNA levels and protein content by Real time- PCR and ELISA. RESULTS: Exercise training decreased blood glucose levels in the DT rats. Diabetes increased the KIF5B and SYD mRNA in both sensory and motor parts and KIF5B content in sciatic nerves in the NTD. Moreover, exercise training modulated the KIF5B and SYD mRNA and KIF5B content to normal levels in the DT. Exercise training in NT rats increased KIF5B and SYD mRNA in sensory and motor parts and KIF5B content in sciatic nerves. CONCLUSIONS: Our results suggest that diabetes seems to change spinal cord KIF5B and SYD mRNA and sciatic nerves KIF5B content and exercise training modifies it, which may be attributable to the training-induced decreased hyperglycemia.
BACKGROUND: Previous research has demonstrated diabetic-induced axonal transport deficits. However, the mechanism of axonal transport impairment induced by diabetes is poorly understood. Kinesin motor proteins have been shown to transport various cargos along highly polarized neurons. In the present study, we investigated the effect of regular treadmill exercise on KIF5B and Sunday Driver (SYD) mRNA levels in sensory and motor parts of spinal cord and KIF5B content in sciatic nerves of streptozotocin (STZ)-induced diabeticrats. METHODS: Forty male Wistar rats were divided into four groups: (1) diabetic trained (DT: n = 10); (2) Non-trained diabetic (NTD: n = 10); (3) normal control (NC: n = 10), and (4) normal trained (NT: n = 10). Two weeks after STZ injection (45 mg/kg, i.p.), the rats were subjected to treadmill exercise for 5 days a week over 6 weeks. We determined mRNA levels and protein content by Real time- PCR and ELISA. RESULTS: Exercise training decreased blood glucose levels in the DTrats. Diabetes increased the KIF5B and SYD mRNA in both sensory and motor parts and KIF5B content in sciatic nerves in the NTD. Moreover, exercise training modulated the KIF5B and SYD mRNA and KIF5B content to normal levels in the DT. Exercise training in NT rats increased KIF5B and SYD mRNA in sensory and motor parts and KIF5B content in sciatic nerves. CONCLUSIONS: Our results suggest that diabetes seems to change spinal cord KIF5B and SYD mRNA and sciatic nerves KIF5B content and exercise training modifies it, which may be attributable to the training-induced decreased hyperglycemia.