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Fructose suppresses uric acid excretion to the intestinal lumen as a result of the induction of oxidative stress by NADPH oxidase activation

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Title: Fructose suppresses uric acid excretion to the intestinal lumen as a result of the induction of oxidative stress by NADPH oxidase activation
Authors: Kaneko, Chihiro Browse this author
Ogura, Jiro Browse this author
Sasaki, Shunichi Browse this author
Okamoto, Keisuke Browse this author
Kobayashi, Masaki Browse this author →KAKEN DB
Kuwayama, Kaori Browse this author
Narumi, Katsuya Browse this author
Iseki, Ken Browse this author →KAKEN DB
Keywords: Hyperuricemia
Fructose
Uric acid excretion
Breast cancer resistance protein
Oxidative stress
NADPH oxidase
Issue Date: Mar-2017
Publisher: Elsevier
Journal Title: Biochimica et Biophysica Acta (BBA) General subjects
Volume: 1861
Issue: 3
Start Page: 559
End Page: 566
Publisher DOI: 10.1016/j.bbagen.2016.11.042
PMID: 27913188
Abstract: Background: A high intake of fructose increases the risk for hyperuricemia. It has been reported that long-term fructose consumption suppressed renal uric acid excretion and increased serum uric acid level. However, the effect of single administration of fructose on excretion of uric acid has not been clarified. Methods: We used male Wistar rats, which were orally administered fructose (5 g/kg). Those rats were used in each experiment at 12 h after administration. Results: Single administration of fructose suppressed the function of ileal uric acid excretion and had no effect on the function of renal uric acid excretion. Breast cancer resistance protein (BCRP) predominantly contributes to intestinal excretion of uric acid as an active homodimer. Single administration of fructose decreased BCRP homodimer level in the ileum. Moreover, diphenyleneiodonium (DPI), an inhibitor of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox), recovered the suppression of the function of ileal uric acid excretion and the Bcrp homodimer level in the ileum of rats that received single administration of fructose. Conclusions: Single administration of fructose decreases in BCRP homodimer level, resulting in the suppression the function of ileal uric acid excretion. The suppression of the function of ileal uric acid excretion by single administration of fructose is caused by the activation of Nox. The results of our study provide a new insight into the mechanism of fructose-induced hyperuricemia. (C) 2016 Elsevier B.V. All rights reserved.
Rights: © 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
http://creativecommons.org/licenses/by-nc-nd/4.0/
Type: article (author version)
URI: http://hdl.handle.net/2115/68654
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 小林 正紀

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