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

Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2.
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DOI:
10.1038/srep31003
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发表时间:
2016-08-30
期刊:
影响因子:
4.6
通讯作者:
Shinomiya N
Shinomiya N
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Matsuo H;Tsunoda T;Ooyama K;Sakiyama M;Sogo T;Takada T;Nakashima A;Nakayama A;Kawaguchi M;Higashino T;Wakai K;Ooyama H;Hokari R;Suzuki H;Ichida K;Inui A;Fujimori S;Shinomiya N

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为了阐明人类肠道通过ABCG 2排泄尿酸盐的生理和病理生理作用,我们分别对终末期肾病(血液透析)和急性胃肠炎患者中ABCG 2功能失调的常见变体Q126 X(rs72552713)和Q141 K(rs2231142)进行了基因分型。106例血液透析患者中,ABCG 2功能障碍显著增加了血清尿酸(SUA)水平(P = 1.1 × 10−4),这证明了ABCG 2在肠道尿酸排泄中的生理作用,因为他们的尿酸排泄几乎依赖于通过ABCG 2的肠道排泄。此外,无论脱水程度如何,67例急性胃肠炎患者的ABCG 2功能障碍均显著升高了SUA(P = 6.3 × 10−3),这证明了ABCG 2在急性胃肠炎中的病理生理作用。这些发现首次显示了ABCG 2介导的人类肠道尿酸盐排泄,并表明了肠道上皮作为排泄途径以及吸收途径的生理和病理生理重要性。此外,SUA的增加可能是一个有用的标志,不仅脱水,而且上皮损害的肠。
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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