Zakareia Faten A
Department of Physiology, King Khalid University Hospital, Kingdom of Saudi Arabia.
Neurosciences (Riyadh). 2012 Oct;17(4):327-35.
To evaluate plasma levels of adrenomedullin (AM) and ghrelin and their correlation with the electrophysiological changes in diabetic neuropathy.
The current study was conducted from March 2008 to November 2010 at the Clinical Physiology Department, King Abdulaziz University Hospital, King Saud University, Riyadh, Kingdom of Saudi Arabia on 90 females divided into 30 controls (group I), 30 controlled diabetic patients (group II), and 30 with peripheral neuropathy (group III). All electrophysiological and biochemical measurements of AM and ghrelin were investigated.
There was a significant decrease of motor and sensory nerve conduction velocity and prolongation of F wave response of median, ulnar, peroneal, and sural nerves in diabetic patients with neuropathy. Ankle/brachial index (A/BI) showed insignificant change in all groups compared with the control group. There was significant decrease of plasma levels of AM and ghrelin in group III compared with group I. The results revealed that AM and ghrelin were positively correlated with peripheral nerves motor and sensory conduction velocities.
The altered concentration of AM and ghrelin in diabetic neuropathy could indicate a pathophysiological role. The decline of plasma levels of AM and ghrelin in diabetic neuropathy may be a causative factor, they have neuroprotective and vasculoprotective effects, so their lack could induce neuronal injury and advancement of neuropathy, but the precise role of AM and ghrelin in the pathogenesis of diabetic neuropathy is still to be elucidated.
评估血浆肾上腺髓质素(AM)和胃饥饿素水平及其与糖尿病神经病变电生理变化的相关性。
本研究于2008年3月至2010年11月在沙特阿拉伯利雅得沙特国王大学阿卜杜勒阿齐兹国王大学医院临床生理科进行,研究对象为90名女性,分为30名对照组(I组)、30名血糖控制良好的糖尿病患者(II组)和30名患有周围神经病变的患者(III组)。对AM和胃饥饿素进行了所有电生理和生化测量。
患有神经病变的糖尿病患者的正中神经、尺神经、腓总神经和腓肠神经的运动和感觉神经传导速度显著降低,F波反应延长。与对照组相比,所有组的踝肱指数(A/BI)变化不显著。与I组相比,III组的血浆AM和胃饥饿素水平显著降低。结果显示,AM和胃饥饿素与周围神经运动和感觉传导速度呈正相关。
糖尿病神经病变中AM和胃饥饿素浓度的改变可能表明其具有病理生理作用。糖尿病神经病变中血浆AM和胃饥饿素水平的下降可能是一个致病因素,它们具有神经保护和血管保护作用,因此它们的缺乏可能导致神经元损伤和神经病变进展,但AM和胃饥饿素在糖尿病神经病变发病机制中的具体作用仍有待阐明。