Thiazolidinediones and Edema: Recent Advances in the Pathogenesis of Thiazolidinediones-Induced Renal Sodium Retention
-
- Shoko Horita
- Department of Internal Medicine, The University of Tokyo Hospital, Tokyo 113-0033, Japan
-
- Motonobu Nakamura
- Department of Internal Medicine, The University of Tokyo Hospital, Tokyo 113-0033, Japan
-
- Nobuhiko Satoh
- Department of Internal Medicine, The University of Tokyo Hospital, Tokyo 113-0033, Japan
-
- Masashi Suzuki
- Department of Internal Medicine, The University of Tokyo Hospital, Tokyo 113-0033, Japan
-
- George Seki
- Department of Internal Medicine, The University of Tokyo Hospital, Tokyo 113-0033, Japan
この論文をさがす
説明
<jats:p>Thiazolidinediones (TZDs) are one of the major classes of antidiabetic drugs that are used widely. TZDs improve insulin resistance by activating peroxisome proliferator-activated receptor gamma (PPAR<jats:italic>γ</jats:italic>) and ameliorate diabetic and other nephropathies, at least, in experimental animals. However, TZDs have side effects, such as edema, congestive heart failure, and bone fracture, and may increase bladder cancer risk. Edema and heart failure, which both probably originate from renal sodium retention, are of great importance because these side effects make it difficult to continue the use of TZDs. However, the pathogenesis of edema remains a matter of controversy. Initially, upregulation of the epithelial sodium channel (ENaC) in the collecting ducts by TZDs was thought to be the primary cause of edema. However, the results of other studies do not support this view. Recent data suggest the involvement of transporters in the proximal tubule, such as sodium-bicarbonate cotransporter and sodium-proton exchanger. Other studies have suggested that sodium-potassium-chloride cotransporter 2 in the thick ascending limb of Henle and aquaporins are also possible targets for TZDs. This paper will discuss the recent advances in the pathogenesis of TZD-induced sodium reabsorption in the renal tubules and edema.</jats:p>
収録刊行物
-
- PPAR Research
-
PPAR Research 2015 1-7, 2015
Wiley