Insulin secretory responses to rising and falling glucose concentrations are delayed in subjects with impaired glucose tolerance |
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Authors: | Ehrmann D A Breda E Cavaghan M K Bajramovic S Imperial J Toffolo G Cobelli C Polonsky K S |
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Institution: | (1) Department of Medicine, Section of Endocrinology, The University of Chicago Pritzker School of Medicine, Chicago, Illinois, USA, US;(2) Department of Electronics and Informatics, University of Padua, Padua, Italy, IT;(3) Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA, US |
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Abstract: | Aims/hypothesis. We hypothesized that beta-cell responses to changes in glucose would not be normal in subjects with impaired glucose tolerance
(IGT). Methods. Three groups of 6 subjects were studied: normal weight with normal glucose tolerance (control subjects); obese with normal
glucose tolerance (Obese-NGT); and obese with IGT (Obese-IGT). All subjects had a graded glucose infusion protocol to increase
(step-up) and then decrease (step-down) plasma glucose. We obtained average insulin-secretion rates (ISR) over the glucose
range common to all three groups during step-up and step-down phases, minimal model indices of beta-cell function (fb, fd, fs, Tup, Tdown ), and insulin sensitivity (Si). Results. ISR differed significantly between step-up and -down phases only in Obese-IGT individuals. Basal (fb) and stimulated (fd, fs) beta-cell sensitivity to glucose were similar in the three groups. Delays between glucose stimulus and beta-cell response
during both step-up (Tup) and -down (Tdown) phases were higher in Obese-IGT compared to Controls and Obese-NGT individuals. The product ISR × Si (10–5·min–2× l) was lower in Obese-IGT compared to Controls, both during step-up (919 ± 851 vs 3192 ± 1185, p < 0.05) and step-down (1455 ± 1203 vs 3625 ± 691, p < 0.05) phases. Consistently, the product fs× Si (10–14·min–2· pmol–1× l) was lower in Obese-IGT than in control subjects (27.6 ± 25.4 vs 103.1 ± 20.2, p < 0.05). Conclusion/interpretation. Subjects with IGT are not able to secrete insulin to compensate adequately for insulin resistance. They also show delays
in the timing of the beta-cell response to glucose when glucose levels are either rising or falling. Diabetologia (2002)
45: ▪–▪]
Received: 30 July 2001 and in revised form: 21 November 2001 |
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Keywords: | Minimal model insulin secretion impaired glucose tolerance pancreatic beta cell |
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