Source:http://linkedlifedata.com/resource/pubmed/id/11815483
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:dateCreated |
2002-3-7
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| pubmed:abstractText |
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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0012-1797
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
51 Suppl 1
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
S221-6
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:11815483-Adult,
pubmed-meshheading:11815483-Blood Glucose,
pubmed-meshheading:11815483-Body Weight,
pubmed-meshheading:11815483-C-Peptide,
pubmed-meshheading:11815483-Diabetes Mellitus, Type 2,
pubmed-meshheading:11815483-Eating,
pubmed-meshheading:11815483-Humans,
pubmed-meshheading:11815483-Insulin,
pubmed-meshheading:11815483-Islets of Langerhans,
pubmed-meshheading:11815483-Male,
pubmed-meshheading:11815483-Models, Biological
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| pubmed:year |
2002
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| pubmed:articleTitle |
Assessing insulin secretion by modeling in multiple-meal tests: role of potentiation.
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| pubmed:affiliation |
C.N.R. (National Research Council) Institute of Systems Science and Biomedical Engineering, Padua, Italy. mari@ladseb.pd.cnr.it
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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