{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:52:16Z","timestamp":1792788736988,"version":"4.5.0"},"reference-count":31,"publisher":"American Diabetes Association","issue":"9","license":[{"start":{"date-parts":[[2025,7,8]],"date-time":"2025-07-08T00:00:00Z","timestamp":1751932800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.diabetesjournals.org\/journals\/pages\/license"}],"funder":[{"name":"AstraZeneca Pharmaceuticals"},{"name":"NIH\/NIDDK","award":["RO1-DK107680-05"],"award-info":[{"award-number":["RO1-DK107680-05"]}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,9,1]]},"abstract":"<jats:sec>\n                    <jats:title>OBJECTIVE<\/jats:title>\n                    <jats:p>To examine the effects of sodium\u2013glucose cotransporter 2 inhibitors (SGLT2is) alone or with glucagon-like peptide 1 receptor agonists (GLP-1RAs) on \u03b2-cell function (BCF) in type 2 diabetes. The hypothesis was that an SGLT2i combined with a GLP-1RA provides superior improvement in BCF than either agent alone.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESEARCH DESIGN AND METHODS<\/jats:title>\n                    <jats:p>Ninety patients underwent a 180-min oral glucose tolerance test (OGTT) 1) after one drug dose (acute study) (placebo [n = 15], dapagliflozin [n = 25], exenatide [n = 25], and dapagliflozin\/exenatide [n = 25]) and 2) after 1 and 4 months of therapy. Corrected Matsuda index (cMI) for urinary glucose loss, insulin secretion, and BCF indices were calculated during OGTT.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>In the acute study, mean \u00b1 SEM cMI in dapagliflozin (2.29 \u00b1 0.33), exenatide (2.03 \u00b1 0.12), and dapagliflozin\/exenatide (2.36 \u00b1 0.14) was higher (P &amp;lt; 0.05) than placebo (1.63 \u00b1 0.36). After 1 and 4 months, cMI remained similarly elevated in exenatide and increased further (P &amp;lt; 0.001) in dapagliflozin and dapagliflozin\/exenatide. In the acute study, insulin secretion in dapagliflozin was similar to placebo but higher (P &amp;lt; 0.001 vs. both) in exenatide and dapagliflozin\/exenatide. After 1 and 4 months in exenatide and in dapagliflozin\/exenatide, insulin secretion remained higher (P &amp;lt; 0.01 vs. both) than dapagliflozin. BCF index in the acute study was 0.40 \u00b1 0.04 in placebo, 62% higher (P &amp;lt; 0.05) in dapagliflozin (0.65 \u00b1 0.10), threefold higher in exenatide (1.17 \u00b1 0.22), and fourfold higher in dapagliflozin\/exenatide (1.69 \u00b1 0.12) (all P &amp;lt; 0.001 vs. placebo). At 1 and 4 months, BCF rose further in dapagliflozin and exenatide but did not increase further in dapagliflozin\/exenatide.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS<\/jats:title>\n                    <jats:p>Dapagliflozin and exenatide monotherapy cause sustained improvements in BCF and insulin sensitivity. Combination therapy with dapagliflozin plus exenatide markedly augmented both BCF and insulin sensitivity above that with either agent alone.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/dc25-0490","type":"journal-article","created":{"date-parts":[[2025,7,8]],"date-time":"2025-07-08T12:59:51Z","timestamp":1751979591000},"page":"1545-1552","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":3,"title":["Changes in \u03b2-Cell Function and Insulin Sensitivity During Treatment With Dapagliflozin Alone or in Combination With Exenatide in Type 2 Diabetes"],"prefix":"10.2337","volume":"48","author":[{"given":"Curtis","family":"Triplitt","sequence":"first","affiliation":[{"name":"Division of Diabetes, Department of Medicine, University of Texas Health Science Center 1 , San Antonio, TX"},{"name":"Texas Diabetes Institute, University Health System 2 , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eugenio","family":"Cersosimo","sequence":"additional","affiliation":[{"name":"Division of Diabetes, Department of Medicine, University of Texas Health Science Center 1 , San Antonio, TX"},{"name":"Texas Diabetes Institute, University Health System 2 , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariam","family":"Alatrach","sequence":"additional","affiliation":[{"name":"Division of Diabetes, Department of Medicine, University of Texas Health Science Center 1 , San Antonio, TX"},{"name":"Texas Diabetes Institute, University Health System 2 , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John","family":"Adams","sequence":"additional","affiliation":[{"name":"Division of Diabetes, Department of Medicine, University of Texas Health Science Center 1 , San Antonio, TX"},{"name":"Texas Diabetes Institute, University Health System 2 , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea","family":"Hansis-Diarte","sequence":"additional","affiliation":[{"name":"Division of Diabetes, Department of Medicine, University of Texas Health Science Center 1 , San Antonio, TX"},{"name":"Texas Diabetes Institute, University Health System 2 , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gozde","family":"Baskoy","sequence":"additional","affiliation":[{"name":"Division of Diabetes, Department of Medicine, University of Texas Health Science Center 1 , San Antonio, TX"},{"name":"Texas Diabetes Institute, University Health System 2 , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amalia","family":"Gastaldelli","sequence":"additional","affiliation":[{"name":"Division of Diabetes, Department of Medicine, University of Texas Health Science Center 1 , San Antonio, TX"},{"name":"Texas Diabetes Institute, University Health System 2 , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alberto","family":"Chavez-Velazquez","sequence":"additional","affiliation":[{"name":"Division of Diabetes, Department of Medicine, University of Texas Health Science Center 1 , San Antonio, TX"},{"name":"Texas Diabetes Institute, University Health System 2 , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8581-6273","authenticated-orcid":false,"given":"Ralph A.","family":"DeFronzo","sequence":"additional","affiliation":[{"name":"Division of Diabetes, Department of Medicine, University of Texas Health Science Center 1 , San Antonio, TX"},{"name":"Texas Diabetes Institute, University Health System 2 , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","published-online":{"date-parts":[[2025,7,8]]},"reference":[{"key":"2026061714341565200_B1","doi-asserted-by":"crossref","first-page":"773","DOI":"10.2337\/db09-9028","article-title":"Banting Lecture. 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