Thiazolidinediones and Edema: Recent Advances in the Pathogenesis of Thiazolidinediones-Induced Renal Sodium Retention
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 (PPARγ) and ameliorate diabetic and other nephropathies, at least, in experimental animals. However, TZDs...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | PPAR Research |
| Online Access: | http://dx.doi.org/10.1155/2015/646423 |
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| author | Shoko Horita Motonobu Nakamura Nobuhiko Satoh Masashi Suzuki George Seki |
| author_facet | Shoko Horita Motonobu Nakamura Nobuhiko Satoh Masashi Suzuki George Seki |
| author_sort | Shoko Horita |
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| description | 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 (PPARγ) 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. |
| format | Article |
| id | doaj-art-d2380500e85d4868bbe5c51987710697 |
| institution | Kabale University |
| issn | 1687-4757 1687-4765 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | PPAR Research |
| spelling | doaj-art-d2380500e85d4868bbe5c519877106972025-02-03T06:06:12ZengWileyPPAR Research1687-47571687-47652015-01-01201510.1155/2015/646423646423Thiazolidinediones and Edema: Recent Advances in the Pathogenesis of Thiazolidinediones-Induced Renal Sodium RetentionShoko Horita0Motonobu Nakamura1Nobuhiko Satoh2Masashi Suzuki3George Seki4Department of Internal Medicine, The University of Tokyo Hospital, Tokyo 113-0033, JapanDepartment of Internal Medicine, The University of Tokyo Hospital, Tokyo 113-0033, JapanDepartment of Internal Medicine, The University of Tokyo Hospital, Tokyo 113-0033, JapanDepartment of Internal Medicine, The University of Tokyo Hospital, Tokyo 113-0033, JapanDepartment of Internal Medicine, The University of Tokyo Hospital, Tokyo 113-0033, JapanThiazolidinediones (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 (PPARγ) 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.http://dx.doi.org/10.1155/2015/646423 |
| spellingShingle | Shoko Horita Motonobu Nakamura Nobuhiko Satoh Masashi Suzuki George Seki Thiazolidinediones and Edema: Recent Advances in the Pathogenesis of Thiazolidinediones-Induced Renal Sodium Retention PPAR Research |
| title | Thiazolidinediones and Edema: Recent Advances in the Pathogenesis of Thiazolidinediones-Induced Renal Sodium Retention |
| title_full | Thiazolidinediones and Edema: Recent Advances in the Pathogenesis of Thiazolidinediones-Induced Renal Sodium Retention |
| title_fullStr | Thiazolidinediones and Edema: Recent Advances in the Pathogenesis of Thiazolidinediones-Induced Renal Sodium Retention |
| title_full_unstemmed | Thiazolidinediones and Edema: Recent Advances in the Pathogenesis of Thiazolidinediones-Induced Renal Sodium Retention |
| title_short | Thiazolidinediones and Edema: Recent Advances in the Pathogenesis of Thiazolidinediones-Induced Renal Sodium Retention |
| title_sort | thiazolidinediones and edema recent advances in the pathogenesis of thiazolidinediones induced renal sodium retention |
| url | http://dx.doi.org/10.1155/2015/646423 |
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