教員業績データベース |
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論文種別 | 原著 |
言語種別 | 英語 |
査読の有無 | 査読あり |
表題 | Iron-restricted pair-feeding affects renal damage in rats with chronic kidney disease. |
掲載誌名 | 正式名:PloS one 略 称:PLoS One ISSNコード:1932-6203(Electronic)1932-6203(Linking) |
掲載区分 | 国外 |
巻・号・頁 | 12(2),pp.e0172157 |
著者・共著者 | Naito Yoshiro, Senchi Aya, Sawada Hisashi, Oboshi Makiko, Horimatsu Tetsuo, Okuno Keisuke, Yasumura Seiki, Ishihara Masaharu, Masuyama Tohru |
発行年月 | 2017/02 |
概要 | BACKGROUND:We have previously shown that dietary iron restriction prevents the development of renal damage in a rat model of chronic kidney disease (CKD). However, iron deficiency is associated with appetite loss. In addition, calorie restriction is reported to prevent the development of end-stage renal pathology in CKD rats. Thus, the beneficial effect of iron restriction on renal damage may depend on calorie restriction. Here, we investigate the effect of pair-feeding iron restriction on renal damage in a rat model of CKD.METHODS:First, to determine the amount of food intake, Sprague-Dawley (SD) rats were randomly given an ad libitum normal diet or an iron-restricted diet, and the food intake was measured. Second, CKD was induced by a 5/6 nephrectomy in SD rats, and CKD rats were given either a pair-feeding normal or iron-restricted diet.RESULTS:Food intake was reduced in the iron-restricted diet group compared to the normal diet group of SD rats for 16 weeks (mean food intake; normal diet group and iron-restricted diet group: 25 and 20 g/day, respectively). Based on the initial experiments, CKD rats received either a pair-feeding normal or iron-restricted diet (20 g/day) for 16 weeks. Importantly, pair-feeding iron restriction prevented the development of proteinuria, glomerulosclerosis, and tubulointerstitial damage in CKD rats. Interestingly, pair-feeding iron restriction attenuated renal expression of nuclear mineralocorticoid receptor in CKD rats.CONCLUSIONS:Pair-feeding iron restriction affected renal damage in a rat model of CKD. |
DOI | 10.1371/journal.pone.0172157 |
PMID | 28196143 |