Delayed Visual Evoked Response is Linked to Vascular Endothelial Growth Factor and Autonomic Dysfunction in Type 2 Diabetes Mellitus

A. Sirisha, Yerrabelli Dhanalakshmi, G. Pal, M. Wyawahare, S. Ahuja
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Abstract

Aims: In this study, we aimed to assess the link between visual evoked potentials (VEP), angiogenic marker (VEGF) and autonomic function tests in type-2 diabetes mellitus (T2DM). Methods: Age-matched 86 male subjects (44 type-2 diabetics on treatment and 42 normal healthy volunteers) were recruited for this study. Body mass index (BMI), basal cardiovascular parameters, spectral analysis of heart rate variability (HRV), were assessed. Fasting blood glucose, insulin, HOMA-IR and VEGF were estimated. The independent association of the P100 latency of VEP with VEGF was determined by multiple regression analysis. Results: LF-HF ratio a marker of sympathovagal balance, increased significantly (p=0.0287) in diabetic group compared to the control group. Comparison of visual evoked potentials between controls and diabetic groups showed significant increase in latency of P100 of both the eyes (right eye p<0.0001, left eye p=0.0003) among the cases. There was significant increase (p=0.0091) in VEGF in diabetic subjects when compared to control. Also positive and significant correlation of P100 latency of VEP with VEGF is seen in diabetics. Conclusions: There is delayed latency of VEP and increased VEGF in type 2 diabetic people. The correlation between VEP and VEGF could indicate the probable role of angiogenesis leading to reduced integrity of the neural pathways in T2DM.
2型糖尿病患者延迟视觉诱发反应与血管内皮生长因子和自主神经功能障碍有关
目的:在本研究中,我们旨在评估2型糖尿病(T2DM)的视觉诱发电位(VEP)、血管生成标志物(VEGF)和自主神经功能测试之间的联系。方法:招募年龄匹配的男性受试者86例,其中治疗中的2型糖尿病患者44例,正常健康志愿者42例。评估身体质量指数(BMI)、基础心血管参数、心率变异性谱分析(HRV)。测定空腹血糖、胰岛素、HOMA-IR和VEGF。通过多元回归分析确定VEP P100潜伏期与VEGF的独立相关性。结果:糖尿病组交感迷走神经平衡指标LF-HF比值显著高于对照组(p=0.0287)。对照组与糖尿病组的视觉诱发电位比较显示,糖尿病组患者双眼P100潜伏期显著增高(右眼p<0.0001,左眼p=0.0003)。与对照组相比,糖尿病患者的VEGF有显著升高(p=0.0091)。糖尿病患者VEP P100潜伏期与VEGF呈显著正相关。结论:2型糖尿病患者VEP潜伏期延迟,VEGF升高。VEP和VEGF之间的相关性可能表明血管生成可能导致T2DM神经通路完整性降低。
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