Assessment of beta-cell function during the oral glucose tolerance test by a minimal model of insulin secretion

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Assessment of beta-cell function during the oral glucose tolerance test by a minimal model of insulin secretion. / Cretti, A.; Lehtovirta, M.; Bonora, E.; Brunato, B.; Zenti, M.G.; Tosi, F.; Caputo, M.; Caruso, B.; Groop, Leif; Muggeo, M.; Bonadonna, R.C.

I: European Journal of Clinical Investigation, Vol. 31, Nr. 5, 2001, s. 405-416.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Harvard

Cretti, A, Lehtovirta, M, Bonora, E, Brunato, B, Zenti, MG, Tosi, F, Caputo, M, Caruso, B, Groop, L, Muggeo, M & Bonadonna, RC 2001, 'Assessment of beta-cell function during the oral glucose tolerance test by a minimal model of insulin secretion', European Journal of Clinical Investigation, vol. 31, nr. 5, s. 405-416. https://doi.org/10.1046/j.1365-2362.2001.00827.x

APA

Cretti, A., Lehtovirta, M., Bonora, E., Brunato, B., Zenti, M. G., Tosi, F., Caputo, M., Caruso, B., Groop, L., Muggeo, M., & Bonadonna, R. C. (2001). Assessment of beta-cell function during the oral glucose tolerance test by a minimal model of insulin secretion. European Journal of Clinical Investigation, 31(5), 405-416. https://doi.org/10.1046/j.1365-2362.2001.00827.x

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Author

Cretti, A. ; Lehtovirta, M. ; Bonora, E. ; Brunato, B. ; Zenti, M.G. ; Tosi, F. ; Caputo, M. ; Caruso, B. ; Groop, Leif ; Muggeo, M. ; Bonadonna, R.C. / Assessment of beta-cell function during the oral glucose tolerance test by a minimal model of insulin secretion. I: European Journal of Clinical Investigation. 2001 ; Vol. 31, Nr. 5. s. 405-416.

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TY - JOUR

T1 - Assessment of beta-cell function during the oral glucose tolerance test by a minimal model of insulin secretion

AU - Cretti, A.

AU - Lehtovirta, M.

AU - Bonora, E.

AU - Brunato, B.

AU - Zenti, M.G.

AU - Tosi, F.

AU - Caputo, M.

AU - Caruso, B.

AU - Groop, Leif

AU - Muggeo, M.

AU - Bonadonna, R.C.

PY - 2001

Y1 - 2001

N2 - Objective To characterise the performance of beta -cell during a standard oral glucose tolerance test (OGTT). Design Fifty-six subjects were studied. A minimal analogic model of beta -cell secretion during the OGTT was applied to all OGTTs (see below). The amount of insulin secreted over 120' in response to oral glucose (OGTT-ISR; Insulin Units 120'(-1) m(-2) BSA) and an index of beta -cell secretory 'force' (beta -lndex; pmol.min(-2).m(-2) BSA) were computed with the aid of the model. In protocol A, 10 healthy subjects underwent two repeat 75 g OGTT with frequent (every 10(/)-15(/)) blood sampling for glucose and C-peptide to test the reproducibility of OGTT-ISR and beta -Index with a complete or a reduced data set. In protocol B, 7 healthy subjects underwent three OGTTs (50, 100 or 150 g), to test the stability of the beta -Index under different glucose loads. In protocol C, 29 subjects (15 with normal glucose tolerance, 7 with impaired glucose tolerance and 7 with newly diagnosed type 2 diabetes) underwent two repeat 75 g OGTT with reduced (every 30' for 120') blood sampling to compare the reproducibility and the discriminant ratio (DR) of OGTT-ISR and beta -index with the insulinogenic index (IG-Index: Delta Insulin (30' - Basal)/Delta Glucose (30' - Basal)). In protocol D, 20 subjects (14 with normal glucose tolerance, 5 with impaired glucose tolerance and 1 with newly-diagnosed type 2 diabetes) underwent a 75 g OGTT and an intravenous glucose tolerance test (IVGTT) on separate days to explore the relationships between acute (0'-10') insulin response (ATR) during the IVGTT and beta -index and OGTT-ISR during the OGTT. Results In all protocols, the minimal analogic model of C-peptide secretion achieved a reasonable fit of the experimental data. In protocol A, a good reproducibility of both beta -index and OGTT-ISR was observed with both complete and reduced (every 30') data sets. In protocol B, increasing the oral glucose load caused progressive increases in OGTT-ISR (from 2.63 +/- 0.70 to 5.11 +/- 0.91 Units.120'(-1).m(-2) BSA; P < 0.01), but the -index stayed the same (4.14 +/- 0.35 vs. 4.29 +/- 0.30 vs. 4.30 +/- 0.33 pmol.min(-2).m(-2) BSA). In protocol C, both OGTT-ISR and beta -index had lower day-to-day CVs (17.6 +/- 2.2 and 12.4 +/- 2.4%, respectively) and higher DRs (2.57 and 1.74, respectively) than the IG-index (CV: 35.5 +/- 6.3%; DR: 0.934). OGTT-ISR was positively correlated to BMI (P < 0.03), whereas -index was inversely related to both fasting and 2 h plasma glucose (P < 0.01 for both). In protocol D, -index, but not OGTT-ISR was significantly correlated to ATR (r = 0.542, P < 0.02). Conclusions Analogically modelling -cell function during the OGTT provides a simple, useful tool for the physiological assessment of beta -cell function.

AB - Objective To characterise the performance of beta -cell during a standard oral glucose tolerance test (OGTT). Design Fifty-six subjects were studied. A minimal analogic model of beta -cell secretion during the OGTT was applied to all OGTTs (see below). The amount of insulin secreted over 120' in response to oral glucose (OGTT-ISR; Insulin Units 120'(-1) m(-2) BSA) and an index of beta -cell secretory 'force' (beta -lndex; pmol.min(-2).m(-2) BSA) were computed with the aid of the model. In protocol A, 10 healthy subjects underwent two repeat 75 g OGTT with frequent (every 10(/)-15(/)) blood sampling for glucose and C-peptide to test the reproducibility of OGTT-ISR and beta -Index with a complete or a reduced data set. In protocol B, 7 healthy subjects underwent three OGTTs (50, 100 or 150 g), to test the stability of the beta -Index under different glucose loads. In protocol C, 29 subjects (15 with normal glucose tolerance, 7 with impaired glucose tolerance and 7 with newly diagnosed type 2 diabetes) underwent two repeat 75 g OGTT with reduced (every 30' for 120') blood sampling to compare the reproducibility and the discriminant ratio (DR) of OGTT-ISR and beta -index with the insulinogenic index (IG-Index: Delta Insulin (30' - Basal)/Delta Glucose (30' - Basal)). In protocol D, 20 subjects (14 with normal glucose tolerance, 5 with impaired glucose tolerance and 1 with newly-diagnosed type 2 diabetes) underwent a 75 g OGTT and an intravenous glucose tolerance test (IVGTT) on separate days to explore the relationships between acute (0'-10') insulin response (ATR) during the IVGTT and beta -index and OGTT-ISR during the OGTT. Results In all protocols, the minimal analogic model of C-peptide secretion achieved a reasonable fit of the experimental data. In protocol A, a good reproducibility of both beta -index and OGTT-ISR was observed with both complete and reduced (every 30') data sets. In protocol B, increasing the oral glucose load caused progressive increases in OGTT-ISR (from 2.63 +/- 0.70 to 5.11 +/- 0.91 Units.120'(-1).m(-2) BSA; P < 0.01), but the -index stayed the same (4.14 +/- 0.35 vs. 4.29 +/- 0.30 vs. 4.30 +/- 0.33 pmol.min(-2).m(-2) BSA). In protocol C, both OGTT-ISR and beta -index had lower day-to-day CVs (17.6 +/- 2.2 and 12.4 +/- 2.4%, respectively) and higher DRs (2.57 and 1.74, respectively) than the IG-index (CV: 35.5 +/- 6.3%; DR: 0.934). OGTT-ISR was positively correlated to BMI (P < 0.03), whereas -index was inversely related to both fasting and 2 h plasma glucose (P < 0.01 for both). In protocol D, -index, but not OGTT-ISR was significantly correlated to ATR (r = 0.542, P < 0.02). Conclusions Analogically modelling -cell function during the OGTT provides a simple, useful tool for the physiological assessment of beta -cell function.

U2 - 10.1046/j.1365-2362.2001.00827.x

DO - 10.1046/j.1365-2362.2001.00827.x

M3 - Article

VL - 31

SP - 405

EP - 416

JO - European Journal of Clinical Investigation

JF - European Journal of Clinical Investigation

SN - 0014-2972

IS - 5

ER -