{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T01:46:38Z","timestamp":1792201598170,"version":"4.4.0"},"reference-count":25,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T00:00:00Z","timestamp":1775520000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T00:00:00Z","timestamp":1775520000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100004336","name":"Novartis","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004336","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001065","name":"Australian Diabetes Society","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","award":["APP10066835"],"award-info":[{"award-number":["APP10066835"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["dom-pubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Glucose\u2010dependent insulinotropic polypeptide (GIP) may exert both insulinotropic and glucagonotropic effects. While its insulinotropic action is reportedly attenuated or abolished with worsening of glycaemic control in type 2 diabetes (T2D), the relationship between GIP and glucagon secretion across different levels of glycaemic control remains unclear. This study evaluated the relationship between postprandial GIP and glucagon responses to a mixed meal in T2D and to intraduodenal fat and glucose infusion in healthy and\/or T2D individuals.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>\n                      Data were analysed from three clinical studies: mixed\u2010meal testing in T2D (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200979), intraduodenal fat infusion (2\u2009kcal\/min over 120\u2009min) in T2D (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200915) and intraduodenal glucose infusion (2\u2009kcal\/min over 60\u2009min) in health and T2D (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200910 each). Relationships between postprandial GIP and glucagon or insulin following the mixed meal were also determined after stratification by HbA1c (&lt;\u20096.5%, 6.5%\u20137.0%, &gt;\u20097.0%).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Following mixed\u2010meal ingestion, early postprandial (0\u201330\u2009min) glucagon secretion correlated positively with GIP, with the strength of this association increasing with higher HbA1c levels. In contrast, the insulinogenic index correlated with GIP only in subgroups with HbA1c &lt;\u20096.5% and between 6.5%\u20137.0%. During intraduodenal fat infusion, glucagon and GIP responses correlated strongly in T2D. Following intraduodenal glucose infusion, early glucagon and GIP increments (0\u201315\u2009min) were closely related in T2D, but not in healthy individuals.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These observations indicate a glycaemia\u2010dependent shift in endogenous GIP action in T2D, characterised by attenuation of insulinotropic effects and relative amplification of glucagonotropic effects with deteriorating glycaemic control.<\/jats:p>\n                    <jats:p>\n                      <jats:bold>Trial Registration:<\/jats:bold>\n                      ACTRN12614001131640, ACTRN12614001117606 and ACTRN12615001240538\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dom.70735","type":"journal-article","created":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T07:23:31Z","timestamp":1775546611000},"page":"5287-5293","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Chronic Glycaemic Control Modulates the Relationship Between\n                    <scp>GIP<\/scp>\n                    and Glucagon Secretion Following Oral and Enteral Nutrients in Type 2 Diabetes"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-1164-4270","authenticated-orcid":false,"given":"Zhenxi","family":"Wang","sequence":"first","affiliation":[{"name":"School of Medicine, College of Health Adelaide University  Adelaide Australia"},{"name":"Centre of Research in Translating Nutritional Science to Good Health Adelaide University  Adelaide Australia"},{"name":"College of Medicine and Public Health Flinders University  Adelaide 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