{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T05:24:37Z","timestamp":1790659477833,"version":"4.1.0"},"reference-count":47,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,3,24]],"date-time":"2018-03-24T00:00:00Z","timestamp":1521849600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabetes Metabolism Res"],"published-print":{"date-parts":[[2018,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Although the ability of glucose to mediate its own in vivo metabolism is long documented, the quantitative measurement of whole body glucose\u2010mediated glucose disposal at basal insulin levels (glucose effectiveness [GE]), followed the introduction of the Minimal Model intravenous glucose tolerance test technique.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A literature review, combined with our own studies, of the role of GE in glucose metabolism in normal and \u201cat risk\u201d individuals, was undertaken to determine GE's contribution to glucose homeostasis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>GE accounts for ~45% to 65% of glucose disposal in man. A negative association between GE and insulin meditated glucose disposal (Si), is present in normal subjects without a family history of type 2 diabetes mellitus but is absent in normoglycaemic \u201cat risk\u201d relatives with a positive family history of diabetes mellitus. Intracellular GE disposal is mediated by mass action of glucose through the skeletal muscle membrane via facilitated Glut 4 transporters. However, GE is frequently forgotten as a significant contributor to the development of glucose intolerance in \u201cat risk\u201d individuals. Only limited studies have examined the role of a lower GE in such normoglycemic subjects with preexisting mild insulin resistance and \u03b2\u2010cell dysfunction. These studies demonstrate that in \u201cat risk\u201d individuals, an initial low GE is a key contributor and predictor of future glucose intolerance, whereas an initial raised GE is protective against future glucose intolerance.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In \u201cat risk\u201d individuals, a low GE and genetically determined vulnerable \u03b2\u2010cell function are more critical determinants of future glucose intolerance than their preexisting insulin\u2010resistant state.<\/jats:p><\/jats:sec>","DOI":"10.1002\/dmrr.2989","type":"journal-article","created":{"date-parts":[[2018,2,16]],"date-time":"2018-02-16T13:52:40Z","timestamp":1518789160000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Glucose effectiveness is a critical pathogenic factor leading to glucose intolerance and type 2 diabetes: An ignored 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