{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T20:52:16Z","timestamp":1791579136490,"version":"4.3.4"},"reference-count":53,"publisher":"American Diabetes Association","issue":"10","license":[{"start":{"date-parts":[[2026,7,24]],"date-time":"2026-07-24T00:00:00Z","timestamp":1784851200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.diabetesjournals.org\/journals\/pages\/license"}],"funder":[{"name":"Bioinformatics Core","award":["RRID"],"award-info":[{"award-number":["RRID"]}]},{"name":"Bioinformatics Core","award":["SCR 012718"],"award-info":[{"award-number":["SCR 012718"]}]},{"name":"NIH","award":["R01DK128077"],"award-info":[{"award-number":["R01DK128077"]}]},{"name":"NIH","award":["R01DK132068"],"award-info":[{"award-number":["R01DK132068"]}]},{"name":"NIH","award":["R01NS138119"],"award-info":[{"award-number":["R01NS138119"]}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK124344"],"award-info":[{"award-number":["R01DK124344"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK125330"],"award-info":[{"award-number":["R01DK125330"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK141617"],"award-info":[{"award-number":["R01DK141617"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008457","name":"University of Virginia","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008457","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,10,1]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>Glucose-dependent insulinotropic polypeptide (GIP) promotes nutrient storage, but its vascular actions in skeletal muscle remain unclear. To determine whether GIP regulates muscle microvascular perfusion, a key determinant of substrate use, we examined GIP receptor (GIPR) expression in vascular endothelium and assessed GIP effects in\u00a0vivo in chow-fed and high-fat diet (HFD)\u2013fed rats. Overnight-fasted rats received 120-min infusions of saline or GIP, with or without concurrent insulin or glucagon-like peptide 1 (GLP-1). Immunofluorescence microscopy demonstrated clear GIPR expression in conduit, resistance, and microvascular vessel endothelium. GIP alone did not alter muscle microvascular perfusion in either group but completely abolished insulin- and GLP-1\u2013induced microvascular recruitment. In cultured endothelial cells, GIP dose-dependently increased endothelin-1 (ET-1) secretion and suppressed insulin- or GLP-1\u2013stimulated nitric oxide production. Transcriptomic profiling implicated activation of the GIP\u2013angiotensin II type 1 receptor\u2013ET-1 pathway. In conclusion, GIPR is widely expressed in vascular endothelium. While GIP does not independently recruit muscle microvasculature, it antagonizes insulin- and GLP-1\u2013mediated vasodilation, identifying GIP as a conditional regulator of skeletal muscle perfusion and nutrient delivery, consistent with its physiological effect in directing nutrients toward storage depots.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title\/>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Article Highlights<\/jats:title>\n                    <jats:p>Skeletal muscle microvasculature is essential for nutrient delivery and metabolic regulation, but the vascular actions of glucose-dependent insulinotropic polypeptide (GIP) in muscle are unknown. We investigated whether GIP regulates skeletal muscle microvascular perfusion and interacts with insulin and GLP-1 signaling. GIP receptors are expressed in vascular endothelium, yet GIP alone does not increase muscle perfusion and instead antagonizes insulin- and GLP-1\u2013mediated microvascular recruitment via possibly angiotensin II type 1 receptor\u2013dependent endothelin-1\/nitric oxide imbalance. GIP acts as a conditional regulator of skeletal muscle microvascular perfusion, revealing a novel mechanism of tissue-specific incretin regulation of nutrient partitioning.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/db25-1009","type":"journal-article","created":{"date-parts":[[2026,7,24]],"date-time":"2026-07-24T14:10:08Z","timestamp":1784902208000},"page":"1864-1880","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":0,"title":["GIP Acutely Blunts Insulin- and GLP-1\u2013Induced Muscle Microvascular Perfusion"],"prefix":"10.2337","volume":"75","author":[{"given":"Jia","family":"Liu","sequence":"first","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia School of Medicine 1 , Charlottesville, VA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Changzoon","family":"Chun","sequence":"additional","affiliation":[{"name":"Department of 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