http://www.cnr.it/ontology/cnr/individuo/prodotto/ID170148

Assessing insulin secretion by modeling in multiple meal tests: role of potentiation (Articolo in rivista)

Type

Articolo in rivista (Classe)
Prodotto della ricerca (Classe)

Label

Assessing insulin secretion by modeling in multiple meal tests: role of potentiation (Articolo in rivista) (literal)

Anno

2002-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.2337/diabetes.51.2007.S221 (literal)

Alternative label

Mari A.; Tura A.; Gastaldelli A.; Ferrannini E. (2002)
Assessing insulin secretion by modeling in multiple meal tests: role of potentiation
in Diabetes (N.Y.N.Y.); American Diabetes Association, Alexandria (Stati Uniti d'America)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Mari A.; Tura A.; Gastaldelli A.; Ferrannini E. (literal)

Pagina inizio

221 (literal)

Pagina fine

226 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url

http://www.ncbi.nlm.nih.gov/pubmed/11815483?dopt=Citation (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

51 (literal)

Rivista

Diabetes (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note

Suppl.1 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali

6 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

S1 (literal)

Note

ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

1, 2: C.N.R. (National Research Council) Institute of Systems Science and Biomedical Engineering, Padova; 3, 4: C.N.R. Institute of ClinicalPhysiology and Department of Internal Medicine, University of Pisa, Pisa, Italy. (literal)

Titolo

Assessing insulin secretion by modeling in multiple meal tests: role of potentiation (literal)

Abstract

We developed a mathematical model of the glucose control of insulin secretion capable of quantifying beta-cell function from a physiological meal test. The model includes a static control, i.e., a secretion component that is a function of plasma glucose concentration (the dose-response function), and a dynamic control, i.e., a secretion component that is proportional to the positive values of the glucose concentration derivative. Furthermore, the dose-response function is assumed to be modulated by a time-varying potentiation factor. To test the model, nine nondiabetic control subjects and nine type 2 diabetic patients received three standardized mixed meals over a period of 14-15 h. Blood samples were drawn for the measurement of glucose, insulin, and C-peptide concentration. The dose-response function, the parameter of the dynamic control, and the potentiation factor were determined by fitting the model to glucose and C-peptide concentrations. In diabetic patients, the dose-response function was shifted to the right (glucose concentration at a reference insulin secretion of 300 pmol.min(-1).m(-2) was 11.7 +/- 1.1 vs. 7.2 +/- 0.7 mmol/l; P < 0.05), and decreased in slope (53 +/- 15 vs. 148 +/- 38 pmol.min(-1).m(-2).mmol(-1).l; P < 0.05) and the parameter of the dynamic control was decreased (220 +/- 67 vs. 908 +/- 276 pmol.m(-2).mmol(-1).l; P < 0.05) compared with the nondiabetic control subjects. Furthermore, potentiation was markedly blunted and delayed: maximum potentiation was observed at the first meal in normal subjects and at the second meal (about 4 h later) in diabetic subjects; the mean time for the potentiation factor was higher (7.1 +/- 0.2 vs. 5.9 +/- 0.2 h; P < 0.01), and the size of potentiation was reduced (2.6 +/- 0.5 vs. 7.2 +/- 1.5 fold increase; P < 0.005). In conclusion, our model of insulin secretion extracts multiple indexes of beta-cell function from a physiological meal test. Use of the model in patients with type 2 diabetes retrieves known defects in insulin secretion but also uncovers new facets of beta-cell dysfunction. (literal)

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