Endocrinology, Austin Health, Heidelberg, Victoria, Australia.
Department of Human Neurotransmitters Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
BMJ Open Diabetes Res Care. 2019 Mar 25;7(1):e000606. doi: 10.1136/bmjdrc-2018-000606. eCollection 2019.
Low sodium intake may trigger sympathetic nervous system (SNS) activation and endothelial dysfunction. Studies have not explored these associations along the glucose continuum. Accordingly, we compared endothelial function and SNS activity in individuals with low sodium intake and differing categories of metabolic risk along the glucose continuum. We hypothesized that low sodium intake is associated with (1) impairment of endothelial function and (2) higher SNS activity in individuals with higher metabolic risk.
In this prospective observational study, participants (n=54) with low sodium intake (single 24 hours urine sodium excretion <150 mmol/24 hours) were categorized based on oral glucose tolerance testing as: normal glucose tolerance (NGT, n=10), impaired glucose tolerance (IGT, n=15), treatment naive type 2 diabetes (T2D-) (n=12) or treated type 2 diabetes (T2D+) (n=17). We assessed endothelial function using pulse amplitude tonometry (PAT) derived reactive hyperemic index and PAT ratio; arterial stiffness via augmentation index; muscle sympathetic nerve activity (MSNA) using microneurography; cardiac baroreflex; heart rate; blood pressure; glycosylated hemoglobin A1c (HbA1c) and lipid profile.
Mean (SD) sodium excretion was 110.6 (26) mmol/24 hours. Compared with NGT, IGT and T2D-, the T2D+ group had lower MSNA (p=0.005), PAT ratio (p=0.04) and baroreflex sensitivity (p=0.0002) and an augmented heart rate (p=0.02). The T2D+ group had appropriate mean (SD) glycemic (HbA1c 7.2 (1.72)%), total cholesterol (4.2 (1.0) mmol/L), low-density lipoprotein (2.2 (1.0) mmol/L) and blood pressure (systolic 136 (13), diastolic 78 (12)) (mm Hg) control.
Individuals with T2D+ have impaired endothelial and baroreflex function, despite low sodium intake, appropriately managed cardiometabolic risk factors and lower SNS activity, compared with others along the glucose continuum. Whether low sodium intake is associated with modulation of the sympathovascular profile in T2D requires further investigation.
低钠摄入可能会引发交感神经系统(SNS)激活和内皮功能障碍。研究尚未探讨这些在葡萄糖连续体中的关联。因此,我们比较了低钠摄入以及葡萄糖连续体中不同代谢风险类别的个体的内皮功能和 SNS 活性。我们假设低钠摄入与(1)内皮功能障碍和(2)代谢风险较高的个体 SNS 活性升高有关。
在这项前瞻性观察性研究中,根据口服葡萄糖耐量试验,将低钠摄入(单 24 小时尿钠排泄量<150mmol/24 小时)的参与者(n=54)分为以下几类:正常糖耐量(NGT,n=10)、糖耐量受损(IGT,n=15)、未经治疗的 2 型糖尿病(T2D-)(n=12)或经治疗的 2 型糖尿病(T2D+)(n=17)。我们使用脉搏幅度张力测定法(PAT)衍生的反应性充血指数和 PAT 比值评估内皮功能;使用微神经记录法评估动脉僵硬度;使用微神经记录法评估肌肉交感神经活性(MSNA);评估心脏压力反射;评估心率;评估血压;评估糖化血红蛋白 A1c(HbA1c)和血脂谱。
平均(标准差)钠排泄量为 110.6(26)mmol/24 小时。与 NGT 相比,IGT 和 T2D-,T2D+组的 MSNA(p=0.005)、PAT 比值(p=0.04)和压力反射敏感性(p=0.0002)较低,心率升高(p=0.02)。T2D+组血糖(HbA1c 7.2(1.72)%)、总胆固醇(4.2(1.0)mmol/L)、低密度脂蛋白(2.2(1.0)mmol/L)和血压(收缩压 136(13),舒张压 78(12))(mmHg)控制情况适当。
尽管低钠摄入、适当控制心血管代谢风险因素和较低的 SNS 活性,但与葡萄糖连续体中的其他人相比,T2D+个体的内皮和压力反射功能受损。低钠摄入是否与 T2D 中的交感血管特征的调节有关,还需要进一步研究。