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Meal and oral glucose tests for assessment of beta -cell function: modeling analysis in normal subjects (Articolo in rivista)
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- Label
- Meal and oral glucose tests for assessment of beta -cell function: modeling analysis in normal subjects (Articolo in rivista) (literal)
- Anno
- 2002-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1152/ajpendo.00093.2002 (literal)
- Alternative label
Mari A.; Schmitz O.; Gastaldelli A.; Oestergaard T.; Nyholm B.: Ferrannini E. (2002)
Meal and oral glucose tests for assessment of beta -cell function: modeling analysis in normal subjects
in American journal of physiology: endocrinology and metabolism; American Physiological Society, Bethesda (Stati Uniti d'America)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Mari A.; Schmitz O.; Gastaldelli A.; Oestergaard T.; Nyholm B.: Ferrannini E. (literal)
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- http://www.ncbi.nlm.nih.gov/pubmed/12388151?dopt=Citation (literal)
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- ISI Web of Science (WOS) (literal)
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- 1: Consiglio Nazionale delle Ricerche Institute of Systems Science and Biomedical Engineering,
35127 Padua;
2, 4, 5: Department of Medicine M(Endocrinology and Diabetes), University Hospital, DK-8000 Aarhus, Denmark
3, 6: Department of Internal Medicine and Consiglio Nazionale delle Ricerche Institute, of Clinical Physiology, University of Pisa, 56126 Pisa, Italy (literal)
- Titolo
- Meal and oral glucose tests for assessment of beta -cell function: modeling analysis in normal subjects (literal)
- Abstract
- We investigated beta-cell function and its relationship to insulin sensitivity in 17 normal volunteers. For insulin secretion (derived by C-peptide deconvolution), a mathematical model was applied to 24-h triple-meal tests (MT) as well as oral glucose tolerance tests (OGTT); insulin sensitivity was assessed by the euglycemic insulin clamp technique. The beta-cell model featured a glucose concentration-insulin secretion dose response (characterized by secretion at 5 mM glucose and slope), a secretion component proportional to the glucose concentration derivative, and a time-dependent potentiation factor (modulating the dose response and accounting for effects of sustained hyperglycemia and incretins). The beta-cell dose-response functions estimated from the whole 24-h MT, the first 2 h of the MT, and the OGTT differed systematically, because a different potentiation factor was involved. In fact, potentiation was higher than average during meals (1.6 +/- 0.1-fold during the first meal) and had a different time course in the MT and OGTT. However, if potentiation was accounted for, the 24- and 2-h MT and the OGTT yielded similar dose responses, and most beta-cell function parameters were intercorrelated (r = 0.50-0.86, P < or = 0.05). The potentiation factor was found to be related to plasma glucose-dependent insulin-releasing polypeptide concentrations (r = 0.49, P < 0.0001). Among beta-cell function parameters, only insulin secretion at 5 mM glucose from MT correlated inversely with insulin sensitivity (24-h MT: r = -0.74, P < 0.001; 2-h MT: r = -0.52, P < 0.05), whereas the dose-response slope and the OGTT parameters did not. In nine other subjects, reproducibility of model parameters was evaluated from repeated MTs. Coefficients of variation were generally approximately 20%, but the derivative component was less reproducible. We conclude that our model for the multiple MT yields useful information on beta-cell function, particularly with regard to the role of potentiation. With cautious interpretation, a 2-h MT or a standard OGTT can be used as surrogates of 24-h tests in assessing spontaneous beta-cell function. (literal)
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