title: Moderate exercise training attenuates inflammatory mediators in DRG of Type 1 diabetic rats.
abstract: Painful neuropathy is a long-term and difficult to treat complication of diabetes that affects 25% of diabetic patients and interferes with their quality of life. Unfortunately, available medical treatments are relatively ineffective due to dependency and addiction. Emerging research indicates that moderate-to-vigorous physical activity provides health-related benefits. However, adequate data is not available to determine whether regular exercise would prevent or delay the development of painful neuropathy in subjects with Type 1 diabetes. This study demonstrates the significance of moderate exercise in the amelioration of pain in animals with Type 1 diabetes after 6weeks of exercise paradigm. After initial acclimatization, streptozotocin-diabetic animals were placed in motorized running wheels for 60minperday, for five days a week for 6weeks starting at one week after diabetes. A growing body of evidence suggests that the release of proinflammatory cytokines plays an important role in the development and persistence of pain. This study demonstrates that moderate exercise increases the expression of inhibitory neurotransmitter enkephalin and also reduces the presence of a number of proinflammatory cytokines in the dorsal root ganglia (DRG), subsequently impeding the development of neuropathy along with a decrease in the voltage gated ion channels in the DRG. Overall, the study suggests that exercise may provide an alternate route of treatment of painful neuropathy in Type 1 diabetic subjects by decreasing the use of pain medications, thereby providing a more useful and efficient way for pain management.
authors.affiliation: Department of Neurology, University of Michigan, Ann Arbor, MI, USA.
authors.forename: HaeJee
authors.initials: H
authors.lastname: Yoon
authors.affiliation: Center of Excellence in Diabetes and Obesity, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, TX, USA.
authors.forename: Vikram
authors.initials: V
authors.lastname: Thakur
authors.affiliation: Department of Neurology, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Danielle
authors.initials: D
authors.lastname: Isham
authors.affiliation: Department of Neurology, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Mona
authors.initials: M
authors.lastname: Fayad
authors.affiliation: Center of Excellence in Diabetes and Obesity, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, TX, USA. Electronic address: munmun.chattopadhyay@ttuhsc.edu.
authors.forename: Munmun
authors.initials: M
authors.lastname: Chattopadhyay
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000473:pathology*; D004195:Disease Models, Animal; D005081:Exercise Therapy / Q000379:methods*; D005727:Ganglia, Spinal / Q000378:metabolism*; D005786:Gene Expression Regulation; D006360:Heat-Shock Proteins; D006930:Hyperalgesia / Q000175:diagnosis / Q000209:etiology; D007249:Inflammation / Q000209:etiology* / Q000534:rehabilitation*; D008055:Lipids / Q000097:blood; D008297:Male; D018377:Neurotransmitter Agents / Q000378:metabolism; D017288:Pain Threshold / Q000502:physiology; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D050053:TRPM Cation Channels / Q000378:metabolism; D050916:TRPV Cation Channels / Q000378:metabolism; D013997:Time Factors
chemical_list: D016207:Cytokines; D006360:Heat-Shock Proteins; D008055:Lipids; D018377:Neurotransmitter Agents; D050053:TRPM Cation Channels; D050916:TRPV Cation Channels; C498947:Trpm8 protein, rat; C493922:Trpv1 protein, rat
keywords: Diabetes; Exercise; Inflammation; Neuropathy; Pain