| Literature DB >> 28926857 |
Wen Wen1, Zhaofei Wan1, Dong Zhou1, Juan Zhou1,2, Zuyi Yuan1,2.
Abstract
Background 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. Methods 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). Results 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; P<0.01), whereas dropped considerably when dietary potassium was supplemented (9.7±5.1 pg/mL to 2.0±0.9 pg/mL; P<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, P<0.01; high-salt to potassium supplementation: r=0.703, P<0.01). Based on multivariate regression analysis, plasma IL-17A showed as an independent predictor of IR. Conclusions The amelioration of salt-loading-induced IR by potassium supplementation in participants may be related to the reduction in plasma IL-17A concentration. © Georg Thieme Verlag KG Stuttgart · New York.Entities:
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Year: 2017 PMID: 28926857 DOI: 10.1055/s-0042-101793
Source DB: PubMed Journal: Exp Clin Endocrinol Diabetes ISSN: 0947-7349 Impact factor: 2.949