Wen Wen, Wan Zhaofei, Zhou Dong, Zhou Juan, Yuan Zuyi
Department of Cardiovascular Medicine, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Yanta West Road, Xi'an, Shaanxi, People's Republic of China.
Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University, Ministry of Education, Xi'an, Shaanxi, People's Republic of China.
Exp Clin Endocrinol Diabetes. 2017 Sep;125(8):571-576. doi: 10.1055/s-0042-101793. Epub 2017 Sep 19.
High dietary salt intake contributes to the development of autoimmune/inflammatory diseases including metabolic syndrome (MetS) which potassium supplementation can potentially reverse. T helper (Th) 17 cells as well as its production interleukin (IL)-17A are involved in the pathogenesis of MetS. The polarization of Th17 cells and enhanced IL-17A production induced by high salt might increase the risk of autoimmune/inflammatory diseases. 45 normotensive subjects (aged 29 to 65 years) were enrolled from a rural community of Northern China at random. All of the participants were maintained on a low-salt (3 g/day) diet for 7 days, a high-salt (18 g/day) diet for 7 days, and then a high-salt diet with potassium supplementation (4.5 g/day, KCl) for another 7 days. Insulin resistance (IR) was determined based on the homeostasis model assessment index (HOMA-IR). Participants exhibited increased plasma insulin level, as well as progressed HOMA-IR, during a high-salt diet intervention, which potassium supplementation reversed. Moreover, after salt loading, the plasma IL-17A concentrations increased significantly (4.2±2.1 pg/mL to 9.7±5.1 pg/mL; <0.01), whereas dropped considerably when dietary potassium was supplemented (9.7±5.1 pg/mL to 2.0±0.9 pg/mL; <0.001). Statistically significant correlations were found between changes in HOMA-IR and changes in plasma IL-17A concentrations during the interventions (low- to high-salt: r=0.642, <0.01; high-salt to potassium supplementation: r=0.703, <0.01). Based on multivariate regression analysis, plasma IL-17A showed as an independent predictor of IR. The amelioration of salt-loading-induced IR by potassium supplementation in participants may be related to the reduction in plasma IL-17A concentration.
高盐饮食摄入会促使包括代谢综合征(MetS)在内的自身免疫性/炎症性疾病的发展,而补充钾可能会逆转这种情况。辅助性T细胞(Th)17及其产生的白细胞介素(IL)-17A参与了代谢综合征的发病机制。高盐诱导的Th17细胞极化和IL-17A产生增加可能会增加自身免疫性/炎症性疾病的风险。从中国北方一个农村社区随机招募了45名血压正常的受试者(年龄在29至65岁之间)。所有参与者先维持7天的低盐(3克/天)饮食,再进行7天的高盐(18克/天)饮食,然后再进行7天补充钾(4.5克/天,氯化钾)的高盐饮食。根据稳态模型评估指数(HOMA-IR)来确定胰岛素抵抗(IR)。在高盐饮食干预期间,参与者的血浆胰岛素水平升高,HOMA-IR进展,而补充钾可使其逆转。此外,在盐负荷后,血浆IL-17A浓度显著增加(从4.2±2.1皮克/毫升增至9.7±5.1皮克/毫升;P<0.01),而在补充膳食钾时则大幅下降(从9.7±5.1皮克/毫升降至2.0±0.9皮克/毫升;P<0.001)。在干预期间(低盐至高盐:r=0.642,P<0.01;高盐至补充钾:r=0.703,P<0.01),发现HOMA-IR的变化与血浆IL-17A浓度的变化之间存在统计学显著相关性。基于多变量回归分析,血浆IL-17A显示为IR的独立预测因子。参与者中补充钾对盐负荷诱导的IR的改善可能与血浆IL-17A浓度的降低有关。