The responses of the inflammatory marker, pentraxin 3, to dietary sodium and potassium interventions
The responses of the inflammatory marker, pentraxin 3, to dietary sodium and potassium interventions
复制标题
炎症标记物五聚蛋白 3 对膳食钠和钾干预的反应
DOI:
10.1111/jch.13273
复制
发表时间:
2018-05-01
影响因子:
2.8
通讯作者:
Mu, Jian-Jun
中科院分区:
文献类型:
--
作者:
Hu, Jia-Wen;Wang, Yang;Mu, Jian-Jun
Pentraxin-3 is a sensitive marker of inflammation that plays dual roles, pathogenic and cardioprotective, in the progression of cardiovascular diseases. Inflammation is intimately involved in salt-induced hypertension. We investigated the responses of pentraxin-3 to sodium and potassium supplementation to elucidate the potential role of pentraxin-3 in salt-induced hypertension. A total of 48 participants from northwest China were enrolled. All participants were maintained on a 3-day normal diet, which was sequentially followed by a 7-day low-sodium diet, a 7-day high-sodium diet, and a 7-day high-sodium plus potassium diet. Plasma concentrations of pentraxin-3 were assessed using ELISA. Plasma pentraxin-3 decreased significantly during the low-salt period compared to baseline (0.57 +/- 0.19ng/mL vs 0.72 +/- 0.33ng/mL, P=.012) and increased during the high-salt period (0.68 +/- 0.26ng/mL vs 0.57 +/- 0.19ng/mL, P=.037). Potassium supplementation inhibited salt-induced increase in pentraxin-3 (0.56 +/- 0.21ng/mL vs 0.68 +/- 0.26ng/mL, P=.015). Ln-transformed pentraxin-3 at baseline was inversely correlated with BMI (r=-.349, P=.02), DBP (r=-.414, P=.005), MAP (r=-.360, P=.017). We found a positive correlation between the ln-transformed concentrations of pentraxin-3 and 24-hour urinary sodium during low and high Na+ periods (r=.269, P=.012) and a negative relationship with 24hours urinary potassium excretion during high-salt and high-salt plus potassium periods (r=-.246, P=.02). These correlations remained significant after adjusting for confounders. Pentraxin-3 responses were more prominent in salt-sensitive individuals than salt-resistant individuals. Dietary salt and potassium interventions significantly altered circulating pentraxin-3.