{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T10:09:06Z","timestamp":1792922946077,"version":"4.5.0"},"reference-count":25,"publisher":"American Diabetes Association","issue":"4","license":[{"start":{"date-parts":[[2021,8,28]],"date-time":"2021-08-28T00:00:00Z","timestamp":1630108800000},"content-version":"vor","delay-in-days":4625,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/3.0\/"}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2009,4,1]]},"abstract":"<jats:sec>\n                  <jats:title>OBJECTIVE<\/jats:title>\n                  <jats:p>Dapagliflozin, a novel inhibitor of renal sodium-glucose cotransporter 2, allows an insulin-independent approach to improve type 2 diabetes hyperglycemia. In this multiple-dose study we evaluated the safety and efficacy of dapagliflozin in type 2 diabetic patients.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESEARCH DESIGN AND METHODS<\/jats:title>\n                  <jats:p>Type 2 diabetic patients were randomly assigned to one of five dapagliflozin doses, metformin XR, or placebo for 12 weeks. The primary objective was to compare mean change from baseline in A1C. Other objectives included comparison of changes in fasting plasma glucose (FPG), weight, adverse events, and laboratory measurements.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>After 12 weeks, dapagliflozin induced moderate glucosuria (52\u201385 g urinary glucose\/day) and demonstrated significant glycemic improvements versus placebo (\u0394A1C \u22120.55 to \u22120.90% and \u0394FPG \u221216 to \u221231 mg\/dl). Weight loss change versus placebo was \u22121.3 to \u22122.0 kg. There was no change in renal function. Serum uric acid decreased, serum magnesium increased, serum phosphate increased at higher doses, and dose-related 24-h urine volume and hematocrit increased, all of small magnitude. Treatment-emergent adverse events were similar across all groups.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>Dapagliflozin improved hyperglycemia and facilitates weight loss in type 2 diabetic patients by inducing controlled glucosuria with urinary loss of \u223c200\u2013300 kcal\/day. Dapagliflozin treatment demonstrated no persistent, clinically significant osmolarity, volume, or renal status changes.<\/jats:p>\n               <\/jats:sec>","DOI":"10.2337\/dc08-1863","type":"journal-article","created":{"date-parts":[[2008,12,30]],"date-time":"2008-12-30T04:43:41Z","timestamp":1230612221000},"page":"650-657","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":584,"title":["Sodium-Glucose Cotransport Inhibition With Dapagliflozin in Type 2 Diabetes"],"prefix":"10.2337","volume":"32","author":[{"given":"James F.","family":"List","sequence":"first","affiliation":[{"name":"Global Clinical Research, Bristol-Myers Squibb, Princeton, New Jersey;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vincent","family":"Woo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Manitoba, Winnipeg, Canada;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Enrique","family":"Morales","sequence":"additional","affiliation":[{"name":"Centro de Investigaci\u00f3n Cardiometab\u00f3lica, Aguascalientes, Mexico;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weihua","family":"Tang","sequence":"additional","affiliation":[{"name":"Global Biometric Sciences, Bristol-Myers Squibb, Princeton, New Jersey."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fred T.","family":"Fiedorek","sequence":"additional","affiliation":[{"name":"Global Clinical Research, Bristol-Myers Squibb, Princeton, New Jersey;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","published-online":{"date-parts":[[2008,12,29]]},"reference":[{"key":"2022031220024833400_B1","doi-asserted-by":"crossref","first-page":"131","DOI":"10.2174\/157339906776818569","article-title":"Pathophysiology and treatment of diabetic peripheral neuropathy: the case for diabetic 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