PPAR&#947; Agonist-Induced Fluid Retention Depends on αENaC Expression in Connecting Tubules | Zendy

Yiling Fu | Zendy; Maria Gerasimova | Zendy; Falk Batz | Zendy; Alexander Kuczkowski | Zendy; Yasaman Alam | Zendy; Paul W. Sanders | Zendy; Caroline Ronzaud | Zendy; Edith Hümmler | Zendy; Volker Vallon | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

PPARγ Agonist-Induced Fluid Retention Depends on αENaC Expression in Connecting Tubules

Author(s) -

Yiling Fu,

Maria Gerasimova,

Falk Batz,

Alexander Kuczkowski,

Yasaman Alam,

Paul W. Sanders,

Caroline Ronzaud,

Edith Hümmler,

Volker Vallon

Publication year - 2014

Publication title -

the nephron journals/nephron journals

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.951

H-Index - 72

eISSN - 2235-3186

pISSN - 1660-8151

DOI - 10.1159/000370254

Subject(s) - epithelial sodium channel , endocrinology , medicine , aldosterone , amiloride , rosiglitazone , sodium , receptor , chemistry , organic chemistry

Thiazolidinediones (TZDs, like rosiglitazone (RGZ)) are peroxisome proliferator-activated receptor γ (PPARγ) agonists used to treat type 2 diabetes. Clinical limitations include TZD-induced fluid retention and body weight (BW) increase, which are inhibited by amiloride, an epithelial-sodium channel (ENaC) blocker. RGZ-induced fluid retention is maintained in mice with αENaC knockdown in the collecting duct (CD). Since ENaC in the connecting tubule (CNT) rather than in CD appears to be critical for normal NaCl retention, we aimed to further explore the role of ENaC in CNT in RGZ-induced fluid retention.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research