交感神经迷走神经失衡导致胰岛素抵抗、炎症、血脂异常和氧化应激引起的一级亲属 2 型糖尿病患者的高血压前期状态和心血管风险。
Sympathovagal imbalance contributes to prehypertension status and cardiovascular risks attributed by insulin resistance, inflammation, dyslipidemia and oxidative stress in first degree relatives of type 2 diabetics.
机构信息
Department of Physiology, Jawaharlal Institute of Post-graduate Medical Education and Research (JIPMER), Puducherry, India.
出版信息
PLoS One. 2013 Nov 12;8(11):e78072. doi: 10.1371/journal.pone.0078072. eCollection 2013.
BACKGROUND
Though cardiovascular (CV) risks are reported in first-degree relatives (FDR) of type 2 diabetics, the pathophysiological mechanisms contributing to these risks are not known. We investigated the association of sympathovagal imbalance (SVI) with CV risks in these subjects.
SUBJECTS AND METHODS
Body mass index (BMI), basal heart rate (BHR), blood pressure (BP), rate-pressure product (RPP), spectral indices of heart rate variability (HRV), autonomic function tests, insulin resistance (HOMA-IR), lipid profile, inflammatory markers, oxidative stress (OS) marker, rennin, thyroid profile and serum electrolytes were measured and analyzed in subjects of study group (FDR of type 2 diabetics, n = 72) and control group (subjects with no family history of diabetes, n = 104).
RESULTS
BMI, BP, BHR, HOMA-IR, lipid profile, inflammatory and OS markers, renin, LF-HF (ratio of low-frequency to high-frequency power of HRV, a sensitive marker of SVI) were significantly increased (p<0.0001) in study group compared to the control group. SVI in study group was due to concomitant sympathetic activation and vagal inhibition. There was significant correlation and independent contribution of markers of insulin resistance, dyslipidemia, inflammation and OS to LF-HF ratio. Multiple-regression analysis demonstrated an independent contribution of LF-HF ratio to prehypertension status (standardized beta 0.415, p<0.001) and bivariate logistic-regression showed significant prediction (OR 2.40, CI 1.128-5.326, p = 0.002) of LF-HF ratio of HRV to increased RPP, the marker of CV risk, in study group.
CONCLUSION
SVI in FDR of type 2 diabetics occurs due to sympathetic activation and vagal withdrawal. The SVI contributes to prehypertension status and CV risks caused by insulin resistance, dyslipidemia, inflammation and oxidative stress in FDR of type 2 diabetics.
背景
尽管已有研究报道 2 型糖尿病患者一级亲属（FDR）存在心血管（CV）风险，但导致这些风险的病理生理机制尚不清楚。我们研究了自主神经失衡（SVI）与这些受试者 CV 风险之间的关系。
受试者和方法
在研究组（2 型糖尿病 FDR，n=72）和对照组（无糖尿病家族史的受试者，n=104）中测量并分析了体质指数（BMI）、基础心率（BHR）、血压（BP）、心率变异性（HRV）的频域指标、自主神经功能测试、胰岛素抵抗（HOMA-IR）、血脂谱、炎症标志物、氧化应激（OS）标志物、肾素、甲状腺功能和血清电解质。
结果
与对照组相比，研究组的 BMI、BP、BHR、HOMA-IR、血脂谱、炎症和 OS 标志物、肾素、LF-HF（HRV 低频与高频功率比，SVI 的敏感标志物）显著增加（p<0.0001）。研究组的 SVI 是由于交感神经兴奋和迷走神经抑制同时存在所致。胰岛素抵抗、血脂异常、炎症和 OS 的标志物与 LF-HF 比值存在显著相关性，且独立相关。多元回归分析显示 LF-HF 比值对高血压前期状态有独立贡献（标准化β 0.415，p<0.001），双变量逻辑回归显示 HRV 的 LF-HF 比值对研究组 RPP（CV 风险标志物）增加的预测具有显著意义（OR 2.40，CI 1.128-5.326，p=0.002）。
结论
2 型糖尿病 FDR 中存在 SVI 是由于交感神经兴奋和迷走神经传出功能下降所致。SVI 导致了 2 型糖尿病 FDR 中由胰岛素抵抗、血脂异常、炎症和氧化应激引起的高血压前期状态和 CV 风险。
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