{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T08:36:16Z","timestamp":1792571776482,"version":"4.5.0"},"reference-count":0,"publisher":"American Diabetes Association","issue":"4","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1998,4,1]]},"abstract":"<jats:p>Islet amyloid is a characteristic feature of type 2 diabetes. Its major component is the normal beta-cell secretory product amylin, or islet amyloid polypeptide (IAPP). To determine whether increased or disproportionate release of amylin may explain the propensity for amyloid deposition in type 2 diabetes, we measured plasma amylin-like immunoreactivity (ALI) and immunoreactive insulin (IRI) release in response to an oral glucose load in 94 Japanese-American subjects with normal glucose tolerance (NGT; n=56), impaired glucose tolerance (IGT; n=10), and type 2 diabetes (n=28) as defined by World Health Organization criteria. The incremental increase in ALI, IRI, and glucose (G) at 30 min after oral glucose ingestion was used to calculate deltaALI\/deltaG and deltaIRI\/deltaG as measures of beta-cell function. Overall glucose metabolism was assessed as the incremental glucose area (glucose AUC) during the 2 h of the oral glucose tolerance test. As expected, plasma glucose concentrations at both fasting (NGT, 5.0+\/-0.4; IGT, 5.5+\/-0.1; type 2 diabetes, 6.2+\/-0.3 mmol\/l; P &amp;lt; 0.0001) and 2 h (NGT, 6.7+\/-0.1; IGT, 9.4+\/-0.3; type 2 diabetes, 13.2 +\/-0.5 mmol\/l; P &amp;lt; 0.0001) were elevated in individuals with IGT and type 2 diabetes. In response to glucose ingestion, plasma IRI and ALI increased in all subjects, but these increments were lower in individuals with reduced glucose tolerance, as reflected in the deltaIRI\/deltaG (NGT, 119+\/-10.3; IGT, 60.7+\/-7.1; type 2 diabetes, 49.7 +\/-5.4 pmol\/l; P &amp;lt; 0.0001) and deltaALI\/deltaG (NGT, 2.6+\/-0.2; IGT, 1.8+\/-0.3; type 2 diabetes, 1.2+\/-0.1 pmol\/l; P &amp;lt; 0.0001). Moreover, these reductions in the 30-min incremental ALI and IRI responses were proportionate such that the molar ratio of ALI to IRI was not different among the three groups (NGT, 2.6+\/-0.2; IGT, 2.9 +\/-0.3; type 2 diabetes, 2.9+\/-0.3%; NS). Further, the relationship between beta-cell function, measured as either deltaIRI\/deltaG or deltaALI\/deltaG, and glucose metabolism, assessed as glucose AUC, was nonlinear and inverse in nature, with r2 values of 0.38 (P &amp;lt; 0.0001) and 0.33 (P &amp;lt; 0.0001), respectively. We conclude that the reduced beta-cell function of IGT and type 2 diabetes includes proportionate reductions in both IRI and ALI release. Thus, it is unlikely that the development of islet amyloid in type 2 diabetes is the result of increased release of ALI.<\/jats:p>","DOI":"10.2337\/diabetes.47.4.640","type":"journal-article","created":{"date-parts":[[2007,3,6]],"date-time":"2007-03-06T19:04:22Z","timestamp":1173207862000},"page":"640-645","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":52,"title":["Reduced amylin release is a characteristic of impaired glucose tolerance and type 2 diabetes in Japanese Americans."],"prefix":"10.2337","volume":"47","author":[{"given":"S E","family":"Kahn","sequence":"first","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, University of Washington and VA Puget Sound Health Care System, Seattle 98108, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C B","family":"Verchere","sequence":"additional","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, University of Washington and VA Puget Sound Health Care System, Seattle 98108, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S","family":"Andrikopoulos","sequence":"additional","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, University of Washington and VA Puget Sound Health Care System, Seattle 98108, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P J","family":"Asberry","sequence":"additional","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, University of Washington and VA Puget Sound Health Care System, Seattle 98108, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D L","family":"Leonetti","sequence":"additional","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, University of Washington and VA Puget Sound Health Care System, Seattle 98108, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P W","family":"Wahl","sequence":"additional","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, University of Washington and VA Puget Sound Health Care System, Seattle 98108, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E J","family":"Boyko","sequence":"additional","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, University of Washington and VA Puget Sound Health Care System, Seattle 98108, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R S","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, University of Washington and VA Puget Sound Health Care System, Seattle 98108, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L","family":"Newell-Morris","sequence":"additional","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, University of Washington and VA Puget Sound Health Care System, Seattle 98108, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W Y","family":"Fujimoto","sequence":"additional","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, University of Washington and VA Puget Sound Health Care System, Seattle 98108, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","container-title":["Diabetes"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.org\/diabetes\/diabetes\/article-pdf\/47\/4\/640\/338632\/9568698.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/diabetesjournals.org\/diabetes\/article-pdf\/47\/4\/640\/338632\/9568698.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,11,2]],"date-time":"2022-11-02T16:44:44Z","timestamp":1667407484000},"score":1,"resource":{"primary":{"URL":"https:\/\/diabetesjournals.org\/diabetes\/article\/47\/4\/640\/11247\/Reduced-amylin-release-is-a-characteristic-of"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1998,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1998,4,1]]}},"URL":"https:\/\/doi.org\/10.2337\/diabetes.47.4.640","relation":{},"ISSN":["0012-1797","1939-327X"],"issn-type":[{"value":"0012-1797","type":"print"},{"value":"1939-327X","type":"electronic"}],"subject":[],"published":{"date-parts":[[1998,4,1]]}}}