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タイトル: Salt loading with unilateral nephrectomy accelerate decline in glomerular filtration rate in the hypertensive, obese, type 2 diabetic SDT fatty rat model of diabetic kidney disease
著者: Shinozaki, Yuichi
Katayama, Yuko
Yamaguchi, Fuminari
Suzuki, Tomohisa
Watanabe, Kana
Uno, Kinuko  kyouindb  KAKEN_id
Tsutsui, Takahiro
Sugimoto, Miki  kyouindb  KAKEN_id
Shinohara, Masami
Miyajima, Katsuhiro
Ohta, Takeshi
著者名の別形: 篠崎, 雄一
筒井, 誉大
杉本, 実紀
太田, 毅
キーワード: GFR decline
salt loading
SDT fatty rat
unilateral nephrectomy
発行日: Apr-2022
出版者: Wiley
誌名: Clinical and Experimental Pharmacology and Physiology
巻: 49
号: 4
開始ページ: 492
終了ページ: 500
抄録: For the evaluation of novel therapeutic agents for diabetic kidney disease (DKD), it is desirable to examine their efficacy in animal models by using the glomerular filtration rate (GFR) as an index. For this purpose, animal models that demonstrate a short-term GFR decline because of disease progression are required. Therefore, we aimed to develop such an animal model of DKD by using obese type 2 diabetic spontaneously diabetic Torii (SDT) fatty rats treated with salt loading by drinking water containing sodium chloride with or without unilateral nephrectomy. As a result, we have found that 0.3% salt loading with unilateral nephrectomy or 0.8% salt loading alone caused a rapid GFR decline, hypertension and rapid development of tubulointerstitial fibrosis. Moreover, the addition of losartan to a mixed diet suppressed the GFR decline in SDT fatty rats treated with 0.3% salt loading with unilateral nephrectomy. These results suggest that the model of SDT fatty rats treated with 0.3% salt loading and unilateral nephrectomy could be used as a hypertensive DKD model for evaluating therapeutic agents based on suppression of GFR decline.
著作権等: This is the peer reviewed version of the following article: [Shinozaki, Y, Katayama, Y, Yamaguchi, F, et al. Salt loading with unilateral nephrectomy accelerates decline in glomerular filtration rate in the hypertensive, obese, type 2 diabetic SDT fatty rat model of diabetic kidney disease. Clin Exp Pharmacol Physiol. 2022; 49: 492– 500.], which has been published in final form at https://doi.org/10.1111/1440-1681.13621. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited.
The full-text file will be made open to the public on 04 February 2023 in accordance with publisher's 'Terms and Conditions for Self-Archiving'.
This is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
URI: http://hdl.handle.net/2433/268906
DOI(出版社版): 10.1111/1440-1681.13621
PubMed ID: 35066915
出現コレクション:学術雑誌掲載論文等

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