{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T06:40:30Z","timestamp":1790404830658,"version":"4.1.0"},"reference-count":53,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2019,2,25]],"date-time":"2019-02-25T00:00:00Z","timestamp":1551052800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100012351","name":"Mitsubishi Tanabe Pharma Corporation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100012351","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Sapporo Medical University","award":["2017-2018"],"award-info":[{"award-number":["2017-2018"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Diabetes Invest"],"published-print":{"date-parts":[[2019,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims\/Introduction<\/jats:title>\n                    <jats:p>Type\u00a02 diabetes mellitus is a risk factor of acute kidney injury after myocardial infarction (MI), a form of cardiorenal syndrome. Recent clinical trials have shown that a sodium\u2013glucose cotransporter\u00a02 (SGLT2) inhibitor improved both cardiac and renal outcomes in patients with type\u00a02 diabetes mellitus, but effects of an SGLT2 inhibitor on cardiorenal syndrome remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>Type\u00a02 diabetes mellitus (Otsuka Long\u2010Evans Tokushima Fatty rats [OLETF]) and control (Long\u2010Evans Tokushima Otsuka rats [LETO]) were treated with canagliflozin, an SGLT2 inhibitor, for 2\u00a0weeks. Renal tissues were analyzed at 12\u00a0h after MI with or without preoperative fasting.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Canagliflozin reduced blood glucose levels in OLETF, and blood \u03b2\u2010hydroxybutyrate levels were increased by canagliflozin only with fasting. MI increased neutrophil gelatinase\u2010associated lipocalin and kidney injury molecule\u20101 protein levels in the kidney by 3.2\u2010 and 1.6\u2010fold, respectively, in OLETF, but not in LETO. The renal messenger ribonucleic acid level of Toll\u2010like receptor\u00a04 was higher in OLETF than in LETO after MI, whereas messenger ribonucleic acid levels of cytokines\/chemokines were not significantly different. Levels of lipid peroxides, nicotinamide adenine dinucleotide phosphate oxidase (NOX)2 and NOX4 proteins after MI were significantly higher in OLETF than in LETO. Canagliflozin with pre\u2010MI fasting suppressed MI\u2010induced renal expression of neutrophil gelatinase\u2010associated lipocalin and kidney injury molecule\u20101 in OLETF, together with reductions in lipid peroxides and NOX proteins in the kidney. Blood \u03b2\u2010hydroxybutyrate levels before MI were inversely correlated with neutrophil gelatinase\u2010associated lipocalin protein levels in OLETF. Pre\u2010incubation with \u03b2\u2010hydroxybutyrate attenuated angiotensin\u00a0II\u2010induced upregulation of NOX4 in NRK\u201052E cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The findings suggest that SGLT2 inhibitor treatment with a fasting period protects kidneys from MI\u2010induced cardiorenal syndrome, possibly by \u03b2\u2010hydroxybutyrate\u2010mediated reduction of NOXs and oxidative stress, in type\u00a02 diabetic rats.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jdi.13009","type":"journal-article","created":{"date-parts":[[2019,1,21]],"date-time":"2019-01-21T03:40:31Z","timestamp":1548042031000},"page":"933-946","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["Canagliflozin, a sodium\u2013glucose cotransporter\u00a02 inhibitor, normalizes renal susceptibility to type\u00a01 cardiorenal syndrome through reduction of renal oxidative stress in diabetic rats"],"prefix":"10.1111","volume":"10","author":[{"given":"Yukishige","family":"Kimura","sequence":"first","affiliation":[{"name":"Department of Cardiovascular, Renal and Metabolic Medicine Sapporo Medical University School of Medicine Sapporo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Atsushi","family":"Kuno","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular, Renal and Metabolic Medicine Sapporo Medical University School of Medicine Sapporo Japan"},{"name":"Department of Pharmacology Sapporo Medical University School of Medicine Sapporo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaya","family":"Tanno","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular, Renal and Metabolic Medicine Sapporo Medical University School of Medicine Sapporo 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