{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T16:32:14Z","timestamp":1792168334594,"version":"4.4.0"},"reference-count":40,"publisher":"American Diabetes Association","issue":"5","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2015,5,1]]},"abstract":"<jats:sec>\n                  <jats:title>OBJECTIVE<\/jats:title>\n                  <jats:p>To investigate the effect of parenteral insulin therapy on endogenous insulin secretion in the Diabetes Prevention Trial\u2013Type 1 (DPT-1).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESEARCH DESIGN AND METHODS<\/jats:title>\n                  <jats:p>In the parenteral insulin arm of DPT-1, subjects without diabetes at high risk of future type 1 diabetes randomized to active treatment received a yearly 4-day intravenous insulin infusion (IV-I) and daily subcutaneous insulin (SC-I). To examine the effects of these insulin therapies on endogenous insulin secretion, C-peptide and glucose levels were compared during oral glucose tolerance tests (OGTTs) performed on and off IV-I and SC-I. Forty-six paired OGTTs were performed in 30 subjects from DPT-1 to determine the effect of IV-I. Twenty paired OGTTs were performed in 15 subjects from DPT-1 to determine the effect of SC-I.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>IV-I suppressed fasting and OGTT-stimulated C-peptide (62% and 40%, respectively), and it significantly lowered fasting glucose (67.4 \u00b1 4.5 mg\/dL during IV-I vs. 90.9 \u00b1 1.8 mg\/dL off insulin; P &amp;lt; 0.05). By contrast, post-OGTT glucose levels were significantly higher during IV-I: Glucose during IV-I versus off insulin at 120 min was 203.9 \u00b1 15.1 vs. 151.6 \u00b1 10.2 mg\/dL, respectively (P &amp;lt; 0.05); 49% of OGTTs became transiently diabetic (&amp;gt;200 mg\/dL at 120 min) when receiving IV-I. Fasting glucose was significantly lower when receiving SC-I versus when off insulin (85 \u00b1 3 vs. 94 \u00b1 2 mg\/dL, respectively; P &amp;lt; 0.05), but SC-I did not significantly alter fasting or OGTT-stimulated C-peptide compared with being off insulin.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>These data demonstrate that the IV-I used in the DPT-1 markedly suppressed endogenous insulin secretion, which was frequently associated with postprandial glucose intolerance. SC-I, however, did not.<\/jats:p>\n               <\/jats:sec>","DOI":"10.2337\/dc14-1825","type":"journal-article","created":{"date-parts":[[2015,2,27]],"date-time":"2015-02-27T04:08:42Z","timestamp":1425010122000},"page":"891-896","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":8,"title":["The Effect of DPT-1 Intravenous Insulin Infusion and Daily Subcutaneous Insulin on Endogenous Insulin Secretion and Postprandial Glucose Tolerance"],"prefix":"10.2337","volume":"38","author":[{"given":"Wei","family":"Hao","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Metabolism, Endocrinology, and Nutrition, University of Washington, Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carla J.","family":"Greenbaum","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute, Virginia Mason Research Center, Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey P.","family":"Krischer","sequence":"additional","affiliation":[{"name":"Divison of Informatics and Biostatistics, University of South Florida, Tampa, FL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Cuthbertson","sequence":"additional","affiliation":[{"name":"Pediatric Epidemiology Center, University of South Florida, Tampa, FL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer B.","family":"Marks","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes, and Metabolism, University of Miami, Miami, FL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jerry P.","family":"Palmer","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Metabolism, Endocrinology, and Nutrition, University of Washington, Seattle, WA"},{"name":"Department of Veterans Affairs, Puget Sound Health Care System, Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","published-online":{"date-parts":[[2015,2,26]]},"reference":[{"key":"2022031301292589800_B1","doi-asserted-by":"crossref","first-page":"1360","DOI":"10.1056\/NEJM198605223142106","article-title":"Type I diabetes mellitus. 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