{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T14:16:55Z","timestamp":1777558615225,"version":"3.51.4"},"reference-count":28,"publisher":"American Diabetes Association","issue":"12","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2008,12,1]]},"abstract":"<jats:p>OBJECTIVE\u2014Slowing of gastric emptying by hyperglycemia, a physiological response to minimize postprandial hyperglycemia, may be impaired in patients with type 1 diabetes. The causes and consequences on glucose homeostasis are unknown.<\/jats:p><jats:p>RESEARCH DESIGN AND METHODS\u2014Consequences of euglycemia- and hyperglycemia-induced changes in gastric emptying on postprandial glucose fluxes and excursions were studied in 10 healthy subjects and 15 type 1 diabetic subjects after ingestion of a mixed meal using the double isotope approach ([6,6-2H2] and [1-13C]glucose) and scintigraphic measurements of gastric emptying.<\/jats:p><jats:p>RESULTS\u2014Gastric emptying was greater in type 1 diabetic subjects (90\u2013120 min, P &amp;lt; 0.03), and 50% retention times were comparable in healthy subjects and type 1 diabetic subjects (167 \u00b1 8 vs. 152 \u00b1 10, P = 0.32). Hyperglycemia markedly delayed gastric emptying in healthy subjects but did not alter it in type 1 diabetic subjects (50% retention time 222 \u00b1 18 vs. 167 \u00b1 8 min, P = 0.003 and 148 \u00b1 9 vs. 152 \u00b1 10 min, P = 0.51). Plasma islet amyloid polypeptide (IAPP) increased approximately fourfold in healthy subjects (P &amp;lt; 0.001), whereas it was undetectable in type 1 diabetic subjects. IAPP replacement, using the analog pramlintide, in type 1 diabetic subjects slowed gastric emptying to a comparable extent, as did hyperglycemia in healthy subjects (P &amp;lt; 0.14), and greatly reduced postprandial hyperglycemia (P &amp;lt; 00.1). Meal-derived glucose appearance in plasma (10.7 \u00b1 0.5 vs. 6.8 \u00b1 0.7 \u03bcmol \u00b7 kg\u22121 \u00b7 min\u22121, P &amp;lt; 0.001) was reduced, and splanchnic glucose sequestration increased (14.0 \u00b1 3.0 vs. 25.0 \u00b1 6.0%, P = 0.04).<\/jats:p><jats:p>CONCLUSIONS\u2014In patients with type 1 diabetes the ability to delay gastric emptying in response to hyperglycemia is impaired. This impairment contributes to exaggerated rates of meal-derived glucose appearance and, ultimately, postprandial glucose excursions.<\/jats:p>","DOI":"10.2337\/dc07-2446","type":"journal-article","created":{"date-parts":[[2008,11,25]],"date-time":"2008-11-25T23:52:31Z","timestamp":1227657151000},"page":"2325-2331","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":51,"title":["Impaired Hyperglycemia-Induced Delay in Gastric Emptying in Patients With Type 1 Diabetes Deficient for Islet Amyloid Polypeptide"],"prefix":"10.2337","volume":"31","author":[{"given":"Hans J.","family":"Woerle","sequence":"first","affiliation":[{"name":"Department of Internal Medicine II, Grosshadern, Clinical Research Unit, Ludwig Maximilians University, Munich, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Max","family":"Albrecht","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II, Grosshadern, Clinical Research Unit, Ludwig Maximilians University, Munich, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rainer","family":"Linke","sequence":"additional","affiliation":[{"name":"Department of Nuclear Medicine, Grosshadern, Ludwig Maximilians University, Munich, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Silvia","family":"Zschau","sequence":"additional","affiliation":[{"name":"Outpatient Diabetes Center, Munich, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christoph","family":"Neumann","sequence":"additional","affiliation":[{"name":"Outpatient Diabetes Center, Munich, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mathias","family":"Nicolaus","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II, Grosshadern, Clinical Research Unit, Ludwig Maximilians University, Munich, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John E.","family":"Gerich","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Rochester School of Medicine, Rochester, New York"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Burkhard","family":"Go\u0308ke","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II, Grosshadern, Clinical Research Unit, Ludwig Maximilians University, Munich, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joerg","family":"Schirra","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II, Grosshadern, Clinical Research Unit, Ludwig Maximilians University, Munich, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1167","reference":[{"key":"2022031216421099000_R1","doi-asserted-by":"crossref","unstructured":"Woerle HJ, Szoke E, Meyer C, Dostou JM, Wittlin SD, Gosmanov NR, Welle SL, Gerich JE: Mechanisms for abnormal postprandial glucose metabolism in type 2 diabetes. 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