scholarly journals The Effects of Combined Exercise Training (Resistance-Aerobic) on Serum Kinesin and Physical Function in Type 2 Diabetes Patients with Diabetic Peripheral Neuropathy (Randomized Controlled Trials)

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Seyedeh Hoda Seyedizadeh ◽  
Sadegh Cheragh-Birjandi ◽  
Mohammad Reza Hamedi Nia
Keyword(s):  
Type 2 Diabetes ◽  
Peripheral Neuropathy ◽  
Exercise Training ◽  
Physical Function ◽  
Diabetic Peripheral Neuropathy ◽  
Diabetic Patients ◽  
Combined Exercise ◽  
Combined Exercise Training ◽  
Diabetes Patients

Diabetic peripheral neuropathy is one of the most common chronic complications of diabetics which causes nerve damage and muscle strength decrease in patients. This in turn results in imbalance leading to the diabetic patients’ daily activity disparity. The present investigation was conducted to specifically study the effects of combined training (resistance-aerobic) on serum kinesin-1 and physical function in type 2 diabetes patients with diabetic peripheral neuropathy. 24 diabetic neuropathic females were randomly to be selected out and divided into two experimental and control groups. The experimental group received resistance-aerobic training for 3 sessions during eight weeks. The exercise training included resistance exercises with 2-3 sets, 6-7 exercise stations, 8-12 repetitions (reps), and 3-5 minutes of rest in between the exercises, and the aerobic exercises contained 50-65% of heart rate reserve (HRR) for 3 minutes with 30 seconds of rest interval between sets and 5-10 repetitions. Results show that the serum kinesin-1 level and aerobic endurance declined after eight weeks of combined (resistance-aerobic) exercise training, but this decrease was not significant. The upper body strength increased but it was not significant, while the lower body showed a significant strength increase. With regard to the progressive nature of diabetic peripheral neuropathy, it seems that even the little changes resulting from the combined exercise training can be useful. Nevertheless, more research is required in this area.

Cognitive impairment in type 2 diabetes patients with and without diabetic peripheral neuropathy

Neuroreport ◽  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Lili Zhao ◽  
Limei Mao ◽  
Qian Liu ◽  
Xiang Chen ◽  
Xiangdong Tang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cognitive Impairment ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Diabetes Patients

scholarly journals Interactions between and Shared Molecular Mechanisms of Diabetic Peripheral Neuropathy and Obstructive Sleep Apnea in Type 2 Diabetes Patients

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Hong Shen ◽  
Junrong Zhao ◽  
Ying Liu ◽  
Guangdong Sun
Keyword(s):  
Type 2 Diabetes ◽  
Obstructive Sleep Apnea ◽  
Peripheral Neuropathy ◽  
Sleep Apnea ◽  
Diabetic Peripheral Neuropathy ◽  
Molecular Mechanisms ◽  
Nitrosative Stress ◽  
Obstructive Sleep ◽  
Diabetes Patients

Type 2 diabetes (T2D) accounts for about 90% of all diabetes patients and incurs a heavy global public health burden. Up to 50% of T2D patients will eventually develop neuropathy as T2D progresses. Diabetic peripheral neuropathy (DPN) is a common diabetic complication and one of the main causes of increased morbidity and mortality of T2D patients. Obstructive sleep apnea (OSA) affects over 15% of the general population and is associated with a higher prevalence of T2D. Growing evidence also indicates that OSA is highly prevalent in T2D patients probably due to diabetic peripheral neuropathy. However, the interrelations among diabetic peripheral neuropathy, OSA, and T2D hitherto have not been clearly elucidated. Numerous molecular mechanisms have been documented that underlie diabetic peripheral neuropathy and OSA, including oxidative stress, inflammation, endothelin-1, vascular endothelial growth factor (VEGF), accumulation of advanced glycation end products, protein kinase C (PKC) signaling, poly ADP ribose polymerase (PARP), nitrosative stress, plasminogen activator inhibitor-1, and vitamin D deficiency. In this review, we seek to illuminate the relationships among T2D, diabetic peripheral neuropathy, and OSA and how they interact with one another. In addition, we summarize and explain the shared molecular mechanisms involved in diabetic peripheral neuropathy and OSA for further mechanistic investigations and novel therapeutic strategies for attenuating and preventing the development and progression of diabetic peripheral neuropathy and OSA in T2D.

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