Svensson Maria K, Lindmark Stina, Wiklund Urban, Rask Peter, Karlsson Marcus, Myrin Jan, Kullberg Joel, Johansson Lars, Eriksson Jan W
Department of Medical Sciences, Uppsala University Hospital, 751 85, Uppsala, Sweden.
Department of Medicine, Umeå University Hospital, Umeå, Sweden.
Cardiovasc Diabetol. 2016 Jun 28;15:91. doi: 10.1186/s12933-016-0411-8.
To evaluate the role of the autonomic nervous system (ANS) in the development of insulin resistance (IR) and assess the relationship between IR and activity of ANS using power spectrum analysis of heart rate variability (HRV).
Twenty-three healthy first-degree relatives of patients with type 2 diabetes (R) and 24 control subjects without family history of diabetes (C) group-matched for age, BMI and sex were included. Insulin sensitivity (M value) was assessed by hyperinsulinemic (56 mU/m(2)/min) euglycemic clamp. Activity of the ANS was assessed using power spectrum analysis of HRV in long-term recordings, i.e., 24-h ECG monitoring, and in short-term recordings during manoeuvres activating the ANS. Computed tomography was performed to estimate the amount and distribution of abdominal adipose tissue.
Insulin sensitivity (M value, mg/kg lbm/min) did not differ significantly between the R and C groups. Total spectral power (Ptot) and very low-frequency (PVLF) power was lower in R than C during 24 h ECG-recordings (p = 0.02 and p = 0.03). The best fit multiple variable linear regression model (r(2) = 0.37, p < 0.001 for model) indicated that body composition (BMI) and long-term low to high frequency (LF/HF) power ratio (std β = -0.46, p = 0.001 and std β = -0.28, p = 0.003, respectively) were significantly and independently associated with the M value.
Altered heart rate variability, assessed by power spectrum analysis, during everyday life is linked to insulin resistance. The data suggest that an increased ratio of sympathetic to parasympathetic nerve activity, occurring via both inherited and acquired mechanisms, could potentially contribute to the development of type 2 diabetes.
评估自主神经系统(ANS)在胰岛素抵抗(IR)发生发展中的作用,并通过心率变异性(HRV)功率谱分析评估IR与ANS活性之间的关系。
纳入23名2型糖尿病患者的健康一级亲属(R组)和24名无糖尿病家族史的对照者(C组),两组在年龄、体重指数(BMI)和性别上进行匹配。采用高胰岛素(56 mU/m²/min)正常血糖钳夹技术评估胰岛素敏感性(M值)。通过长期记录(即24小时心电图监测)以及激活ANS的操作过程中的短期记录,利用HRV功率谱分析评估ANS活性。进行计算机断层扫描以估计腹部脂肪组织的数量和分布。
R组和C组之间的胰岛素敏感性(M值,mg/kg瘦体重/分钟)无显著差异。在24小时心电图记录期间,R组的总频谱功率(Ptot)和极低频(PVLF)功率低于C组(p = 0.02和p = 0.03)。最佳拟合多变量线性回归模型(模型的r² = 0.37,p < 0.001)表明,身体成分(BMI)和长期低频与高频(LF/HF)功率比(标准化β分别为 -0.46,p = 0.001和标准化β = -0.28,p = 0.003)与M值显著且独立相关。
通过功率谱分析评估的日常生活中心率变异性改变与胰岛素抵抗有关。数据表明,通过遗传和后天机制发生的交感神经与副交感神经活动比值增加可能潜在地促成2型糖尿病的发生发展。