{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T09:25:18Z","timestamp":1790673918700,"version":"4.1.0"},"reference-count":52,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2014,8,6]],"date-time":"2014-08-06T00:00:00Z","timestamp":1407283200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Biopharm &amp; Drug Disp"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Sodium glucose cotransporter 2 (SGLT2) inhibitors have been reported to lower the serum uric acid (SUA) level. To elucidate the mechanism responsible for this reduction, SUA and the urinary excretion rate of uric acid (UE\n                    <jats:sub>UA<\/jats:sub>\n                    ) were analysed after the oral administration of luseogliflozin, a SGLT2 inhibitor, to healthy subjects. After dosing, SUA decreased, and a negative correlation was observed between the SUA level and the UE\n                    <jats:sub>UA<\/jats:sub>\n                    , suggesting that SUA decreased as a result of the increase in the UE\n                    <jats:sub>UA<\/jats:sub>\n                    . The increase in UE\n                    <jats:sub>UA<\/jats:sub>\n                    was correlated with an increase in urinary\n                    <jats:sc>d<\/jats:sc>\n                    \u2010glucose excretion, but not with the plasma luseogliflozin concentration. Additionally,\n                    <jats:italic>in vitro<\/jats:italic>\n                    transport experiments showed that luseogliflozin had no direct effect on the transporters involved in renal UA reabsorption. To explain that the increase in UE\n                    <jats:sub>UA<\/jats:sub>\n                    is likely due to glycosuria, the study focused on the facilitative glucose transporter 9 isoform 2 (GLUT9\u0394N,\n                    <jats:italic>SLC2A9b<\/jats:italic>\n                    ), which is expressed at the apical membrane of the kidney tubular cells and transports both UA and\n                    <jats:sc>d<\/jats:sc>\n                    \u2010glucose. It was observed that the efflux of [\n                    <jats:sup>14<\/jats:sup>\n                    C]UA in\n                    <jats:italic>Xenopus<\/jats:italic>\n                    oocytes expressing the GLUT9 isoform 2 was\n                    <jats:italic>trans<\/jats:italic>\n                    \u2010stimulated by 10 m\n                    <jats:sc>m d<\/jats:sc>\n                    \u2010glucose, a high concentration of glucose that existed under SGLT2 inhibition. On the other hand, the uptake of [\n                    <jats:sup>14<\/jats:sup>\n                    C]UA by oocytes was\n                    <jats:italic>cis<\/jats:italic>\n                    \u2010inhibited by 100 m\n                    <jats:sc>m d<\/jats:sc>\n                    \u2010glucose, a concentration assumed to exist in collecting ducts. In conclusion, it was demonstrated that the UE\n                    <jats:sub>UA<\/jats:sub>\n                    could potentially be increased by luseogliflozin\u2010induced glycosuria, with alterations of UA transport activity because of urinary glucose. \u00a9 2014 The Authors.\n                    <jats:italic>Biopharmaceutics &amp; Drug Disposition<\/jats:italic>\n                    . Published by John Wiley &amp; Sons Ltd.\n                  <\/jats:p>","DOI":"10.1002\/bdd.1909","type":"journal-article","created":{"date-parts":[[2014,7,7]],"date-time":"2014-07-07T16:25:16Z","timestamp":1404750316000},"page":"391-404","source":"Crossref","is-referenced-by-count":334,"title":["SGLT2 inhibitor lowers serum uric acid through alteration of uric acid transport activity in renal tubule by increased glycosuria"],"prefix":"10.1002","volume":"35","author":[{"given":"Yukihiro","family":"Chino","sequence":"first","affiliation":[{"name":"Department of Membrane Transport and Biopharmaceutics, Faculty of Pharmaceutical Sciences, Institute of Medical, Pharmaceutical and Health Sciences Kanazawa University  Kakuma\u2010machi Kanazawa 920\u20101192 Japan"},{"name":"Drug Safety and Pharmacokinetics Laboratories Taisho Pharmaceutical Co., Ltd  1\u2010403 Yoshino\u2010cho Kita\u2010ku Saitama 331\u20109530 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