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Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2

To clarify the physiological and pathophysiological roles of intestinal urate excretion via ABCG2 in humans, we genotyped ABCG2 dysfunctional common variants, Q126X (rs72552713) and Q141K (rs2231142), in end-stage renal disease (hemodialysis) and acute gastroenteritis patients, respectively. ABCG2 d...

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Autores principales: Matsuo, Hirotaka, Tsunoda, Tomoyuki, Ooyama, Keiko, Sakiyama, Masayuki, Sogo, Tsuyoshi, Takada, Tappei, Nakashima, Akio, Nakayama, Akiyoshi, Kawaguchi, Makoto, Higashino, Toshihide, Wakai, Kenji, Ooyama, Hiroshi, Hokari, Ryota, Suzuki, Hiroshi, Ichida, Kimiyoshi, Inui, Ayano, Fujimori, Shin, Shinomiya, Nariyoshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5004129/
https://www.ncbi.nlm.nih.gov/pubmed/27571712
http://dx.doi.org/10.1038/srep31003
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author Matsuo, Hirotaka
Tsunoda, Tomoyuki
Ooyama, Keiko
Sakiyama, Masayuki
Sogo, Tsuyoshi
Takada, Tappei
Nakashima, Akio
Nakayama, Akiyoshi
Kawaguchi, Makoto
Higashino, Toshihide
Wakai, Kenji
Ooyama, Hiroshi
Hokari, Ryota
Suzuki, Hiroshi
Ichida, Kimiyoshi
Inui, Ayano
Fujimori, Shin
Shinomiya, Nariyoshi
author_facet Matsuo, Hirotaka
Tsunoda, Tomoyuki
Ooyama, Keiko
Sakiyama, Masayuki
Sogo, Tsuyoshi
Takada, Tappei
Nakashima, Akio
Nakayama, Akiyoshi
Kawaguchi, Makoto
Higashino, Toshihide
Wakai, Kenji
Ooyama, Hiroshi
Hokari, Ryota
Suzuki, Hiroshi
Ichida, Kimiyoshi
Inui, Ayano
Fujimori, Shin
Shinomiya, Nariyoshi
author_sort Matsuo, Hirotaka
collection PubMed
description To clarify the physiological and pathophysiological roles of intestinal urate excretion via ABCG2 in humans, we genotyped ABCG2 dysfunctional common variants, Q126X (rs72552713) and Q141K (rs2231142), in end-stage renal disease (hemodialysis) and acute gastroenteritis patients, respectively. ABCG2 dysfunction markedly increased serum uric acid (SUA) levels in 106 hemodialysis patients (P = 1.1 × 10(−4)), which demonstrated the physiological role of ABCG2 for intestinal urate excretion because their urate excretion almost depends on intestinal excretion via ABCG2. Also, ABCG2 dysfunction significantly elevated SUA in 67 acute gastroenteritis patients (P = 6.3 × 10(−3)) regardless of the degree of dehydration, which demonstrated the pathophysiological role of ABCG2 in acute gastroenteritis. These findings for the first time show ABCG2-mediated intestinal urate excretion in humans, and indicates the physiological and pathophysiological importance of intestinal epithelium as an excretion pathway besides an absorption pathway. Furthermore, increased SUA could be a useful marker not only for dehydration but also epithelial impairment of intestine.
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spelling pubmed-50041292016-09-07 Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2 Matsuo, Hirotaka Tsunoda, Tomoyuki Ooyama, Keiko Sakiyama, Masayuki Sogo, Tsuyoshi Takada, Tappei Nakashima, Akio Nakayama, Akiyoshi Kawaguchi, Makoto Higashino, Toshihide Wakai, Kenji Ooyama, Hiroshi Hokari, Ryota Suzuki, Hiroshi Ichida, Kimiyoshi Inui, Ayano Fujimori, Shin Shinomiya, Nariyoshi Sci Rep Article To clarify the physiological and pathophysiological roles of intestinal urate excretion via ABCG2 in humans, we genotyped ABCG2 dysfunctional common variants, Q126X (rs72552713) and Q141K (rs2231142), in end-stage renal disease (hemodialysis) and acute gastroenteritis patients, respectively. ABCG2 dysfunction markedly increased serum uric acid (SUA) levels in 106 hemodialysis patients (P = 1.1 × 10(−4)), which demonstrated the physiological role of ABCG2 for intestinal urate excretion because their urate excretion almost depends on intestinal excretion via ABCG2. Also, ABCG2 dysfunction significantly elevated SUA in 67 acute gastroenteritis patients (P = 6.3 × 10(−3)) regardless of the degree of dehydration, which demonstrated the pathophysiological role of ABCG2 in acute gastroenteritis. These findings for the first time show ABCG2-mediated intestinal urate excretion in humans, and indicates the physiological and pathophysiological importance of intestinal epithelium as an excretion pathway besides an absorption pathway. Furthermore, increased SUA could be a useful marker not only for dehydration but also epithelial impairment of intestine. Nature Publishing Group 2016-08-30 /pmc/articles/PMC5004129/ /pubmed/27571712 http://dx.doi.org/10.1038/srep31003 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Matsuo, Hirotaka
Tsunoda, Tomoyuki
Ooyama, Keiko
Sakiyama, Masayuki
Sogo, Tsuyoshi
Takada, Tappei
Nakashima, Akio
Nakayama, Akiyoshi
Kawaguchi, Makoto
Higashino, Toshihide
Wakai, Kenji
Ooyama, Hiroshi
Hokari, Ryota
Suzuki, Hiroshi
Ichida, Kimiyoshi
Inui, Ayano
Fujimori, Shin
Shinomiya, Nariyoshi
Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2
title Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2
title_full Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2
title_fullStr Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2
title_full_unstemmed Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2
title_short Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2
title_sort hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via abcg2
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5004129/
https://www.ncbi.nlm.nih.gov/pubmed/27571712
http://dx.doi.org/10.1038/srep31003
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