{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T05:21:27Z","timestamp":1790400087109,"version":"4.1.0"},"reference-count":30,"publisher":"American Diabetes Association","issue":"4","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2005,4,1]]},"abstract":"<jats:p>Postprandial hyperglycemia and preprandial hypoglycemia contribute to poor glycemic control in type 1 diabetes. We hypothesized that postprandial glycemic excursions could be normalized in type 1 diabetes by suppressing glucagon with pramlintide acetate in the immediate postprandial period and supplementing glucagon in the late postprandial period. A total of 11 control subjects were compared with 8 type 1 diabetic subjects on insulin pump therapy, using the usual insulin bolus\u2013to\u2013carbohydrate ratio during a standard liquid meal. Type 1 diabetic subjects were then randomized to two open-labeled studies. On one occasion, type 1 diabetic subjects received a 60% increase in the insulin bolus\u2013to\u2013carbohydrate ratio with minidose glucagon rescue injections, and on the other occasion type 1 diabetic subjects received 30\u201345 \u03bcg pramlintide with their usual insulin bolus\u2013to\u2013carbohydrate ratio. Glucose, glucagon, amylin (pramlintide), and insulin concentrations were measured for 420 min. The plasma glucose area under the curve (AUC) for 0\u2013420 min was lower in control versus type 1 diabetic subjects (316 \u00b1 5 vs. 929 \u00b1 18 mg \u00b7 h\u22121 \u00b7 dl\u22121, P &amp;lt; 0.0001). Pramlintide, but not an increase in insulin, reduced immediate postprandial hyperglycemia (AUC0\u2013180 min 470 \u00b1 43 vs. 434 \u00b1 48 mg \u00b7 h\u22121 \u00b7 dl\u22121, P &amp;lt; 0.01). Pramlintide administration suppressed glucagon (P &amp;lt; 0.02), and glucagon injections prevented late hypoglycemia with increased insulin. In summary, in type 1 diabetes, glucagon modulation with pramlintide as an adjunct to insulin therapy may prove beneficial in controlling postmeal glycemic swings.<\/jats:p>","DOI":"10.2337\/diabetes.54.4.1100","type":"journal-article","created":{"date-parts":[[2007,3,6]],"date-time":"2007-03-06T19:04:22Z","timestamp":1173207862000},"page":"1100-1107","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":77,"title":["The Role of Amylin and Glucagon in the Dampening of Glycemic Excursions in Children With Type 1 Diabetes"],"prefix":"10.2337","volume":"54","author":[{"given":"Rubina A.","family":"Heptulla","sequence":"first","affiliation":[{"name":"From the Department of Pediatrics, Division of Diabetes and Endocrinology, Texas Children\u2019s Hospital, Baylor College of Medicine, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luisa M.","family":"Rodriguez","sequence":"additional","affiliation":[{"name":"From the Department of Pediatrics, Division of Diabetes and Endocrinology, Texas Children\u2019s Hospital, Baylor College of Medicine, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa","family":"Bomgaars","sequence":"additional","affiliation":[{"name":"From the Department of Pediatrics, Division of Diabetes and Endocrinology, Texas Children\u2019s Hospital, Baylor College of Medicine, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morey W.","family":"Haymond","sequence":"additional","affiliation":[{"name":"From the Department of Pediatrics, Division of Diabetes and Endocrinology, Texas Children\u2019s Hospital, Baylor College of Medicine, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","reference":[{"key":"2022031209292518100_R1","doi-asserted-by":"crossref","unstructured":"The Diabetes Control and Complications Trial Research Group: The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. 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