{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T15:18:26Z","timestamp":1783955906226,"version":"3.55.0"},"reference-count":56,"publisher":"The Endocrine Society","issue":"9","license":[{"start":{"date-parts":[[2022,6,20]],"date-time":"2022-06-20T00:00:00Z","timestamp":1655683200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"American Diabetes Association Innovative and Clinical Translational","award":["1-19-ICTS-068"],"award-info":[{"award-number":["1-19-ICTS-068"]}]},{"DOI":"10.13039\/100000862","name":"Doris Duke Charitable Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000862","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 DK088214"],"award-info":[{"award-number":["R01 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Sciences","doi-asserted-by":"publisher","award":["8UL1TR000170-05"],"award-info":[{"award-number":["8UL1TR000170-05"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,8,18]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Polymorphisms in the gene encoding the glucagon-like peptide-1 receptor (GLP1R) are associated with type 2 diabetes but their effects on incretin levels remain unclear.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>We evaluated the physiologic and hormonal effects of GLP1R genotypes before and after interventions that influence glucose physiology.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Design<\/jats:title>\n                  <jats:p>Pharmacogenetic study conducted at 3 academic centers in Boston, Massachusetts.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Participants<\/jats:title>\n                  <jats:p>A total of 868 antidiabetic drug-na\u00efve participants with type 2 diabetes or at risk for developing diabetes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Interventions<\/jats:title>\n                  <jats:p>We analyzed 5 variants within GLP1R (rs761387, rs10305423, rs10305441, rs742762, and rs10305492) and recorded biochemical data during a 5-mg glipizide challenge and a 75-g oral glucose tolerance test (OGTT) following 4 doses of metformin 500 mg over 2 days.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Main Outcomes<\/jats:title>\n                  <jats:p>We used an additive mixed-effects model to evaluate the association of these variants with glucose, insulin, and incretin levels over multiple timepoints during the OGTT.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>During the OGTT, the G-risk allele at rs761387 was associated with higher total GLP-1 (2.61 pmol\/L; 95% CI, 1.0.72-4.50), active GLP-1 (2.61 pmol\/L; 95% CI, 0.04-5.18), and a trend toward higher glucose (3.63; 95% CI, -0.16 to 7.42 mg\/dL) per allele but was not associated with insulin. During the glipizide challenge, the G allele was associated with higher insulin levels per allele (2.01 IU\/mL; 95% CI, 0.26-3.76). The other variants were not associated with any of the outcomes tested.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>GLP1R variation is associated with differences in GLP-1 levels following an OGTT load despite no differences in insulin levels, highlighting altered incretin signaling as a potential mechanism by which GLP1R variation affects T2D risk.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/clinem\/dgac374","type":"journal-article","created":{"date-parts":[[2022,6,20]],"date-time":"2022-06-20T14:50:47Z","timestamp":1655736647000},"page":"2580-2588","source":"Crossref","is-referenced-by-count":10,"title":["Association of <i>GLP1R<\/i> Polymorphisms With the Incretin Response"],"prefix":"10.1210","volume":"107","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6082-0631","authenticated-orcid":false,"given":"Edgar G","family":"Dorsey-Trevino","sequence":"first","affiliation":[{"name":"Department of Medicine, Harvard Medical School , Boston, MA 02115 , USA"},{"name":"Division of General Internal Medicine, Massachusetts General Hospital , Boston, MA 02114 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Varinderpal","family":"Kaur","sequence":"additional","affiliation":[{"name":"Diabetes Unit and Center for Genomic Medicine, Massachusetts General Hospital , Boston, MA 02114 , USA"},{"name":"Programs in Metabolism and Medical & Population Genetics, Broad Institute of MIT and Harvard , Cambridge, MA 02142 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8494-3660","authenticated-orcid":false,"given":"Josep M","family":"Mercader","sequence":"additional","affiliation":[{"name":"Department of Medicine, Harvard Medical School , Boston, MA 02115 , USA"},{"name":"Diabetes Unit and Center for Genomic Medicine, Massachusetts General 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