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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-3-7
pubmed:abstractText
The availability of quantitative indexes describing beta-cell function in normal life conditions is important for the characterization of impaired mechanisms of insulin secretion in pathophysiological states. Recently, an oral C-peptide minimal model has been proposed and applied to subjects with normal glucose tolerance (NGT) during graded up-and-down glucose infusion protocols (40-min periods at 4, 8, 16, 8, 4, and 0 mg.kg(-1).min(-1)) and oral glucose tolerance tests. These tests are characterized by slow glucose and C-peptide dynamics, which reproduce prandial conditions. In view of the importance of beta-cell dysfunction in the pathogenesis of type 2 diabetes, our aim was to test and use the oral minimal model in subjects with impaired glucose tolerance (IGT) to identify deranged mechanisms of beta-cell function. Plasma C-peptide and glucose data from graded up-and-down glucose infusions were analyzed in nine NGT and four IGT subjects using the classic deconvolution approach and the oral minimal model, and indexes of beta-cell function were derived. An index of insulin sensitivity was also obtained for each subject from minimal model analysis of glucose and insulin levels achieved during the test. Both deconvolution and minimal model analyses revealed that individuals with IGT have a relative defect in the ability to secrete enough insulin to adequately compensate for insulin resistance. Additionally, minimal model analysis suggests that insulin secretory defect in IGT arises from delays in the timing of the beta-cell response to glucose.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
51 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S227-33
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Insulin release in impaired glucose tolerance: oral minimal model predicts normal sensitivity to glucose but defective response times.
pubmed:affiliation
Department of Electronics and Informatics, University of Padua, Padua, Italy.
pubmed:publicationType
Journal Article