http://www.cnr.it/ontology/cnr/individuo/prodotto/ID167845

Predominant role of reduced beta-cell sensitivity to glucose over insulin resistance in impaired glucose tolerance (Articolo in rivista)

Type

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

Label

Predominant role of reduced beta-cell sensitivity to glucose over insulin resistance in impaired glucose tolerance (Articolo in rivista) (literal)

Anno

2003-01-01T00:00:00+01:00 (literal)

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

10.1007/s00125-003-1169-6 (literal)

Alternative label

Ferrannini E.; Gastaldelli A.; Miyazaki Y.; Matsuda M.; Pettiti M.; Natali A.; Mari A.; DeFronzo RA. (2003)
Predominant role of reduced beta-cell sensitivity to glucose over insulin resistance in impaired glucose tolerance
in Diabetologia (Berl.); Springer Verlag, New York NY (Stati Uniti d'America)
(literal)

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

Ferrannini E.; Gastaldelli A.; Miyazaki Y.; Matsuda M.; Pettiti M.; Natali A.; Mari A.; DeFronzo RA. (literal)

Pagina inizio

1211 (literal)

Pagina fine

1219 (literal)

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

L'impiego di un modello matematico per l'analisi quantitativa della funzione di secrezione di insulina da un semplice test clinico ha consentito un'analisi della funzione secretoria nello stato pre-diabetico secondo criteri nuovi nel settore. In particolare l'analsi ha rivelato l'insufficienza di alcuni paradigmi correnti e ha posto le basi per una loro analisi critica di prossima pubblicazione in una review sulla rivista dell'associazione europea per lo studio del diabete. (literal)

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

http://www.ncbi.nlm.nih.gov/pubmed/12879253?dopt=Citation (literal)

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

46 (literal)

Rivista

Diabetologia (Rivista)

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9 (literal)

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

9 (literal)

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L'articolo e` un contributo allo studio del deterioramento della funzione di secrezione di insulina in soggetti pre-diabetici. L'uso di un modello matematico ha reso possibile un'analisi quantitativa dettagliata della funzione secretoria utilizzando un semplice test clinico. (literal)

Note

ISI Web of Science (WOS) (literal)

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

1: Metabolism Unit, C.N.R. Institute of Clinical Physiology and Department of Internal Medicine, University of Pisa School of Medicine, Pisa, Italy / Diabetes Division, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, USA; 2, 5, 6: Metabolism Unit, C.N.R. Institute of Clinical Physiology and Department of Internal Medicine, University of Pisa School of Medicine, Pisa, Italy; 3, 4, 8: Diabetes Division, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, USA; 7: C.N.R. Institute of Biomedical Engineering, Padova, Italy (literal)

Titolo

Predominant role of reduced beta-cell sensitivity to glucose over insulin resistance in impaired glucose tolerance (literal)

Abstract

AIMS/HYPOTHESIS: Impaired glucose tolerance (IGT) is an insulin-resistant state and a risk factor for Type 2 diabetes. The relative roles of insulin resistance and insulin deficiency in IGT have been disputed. METHODS: In 40 IGT subjects and 63 sex-, age-, and weight-matched controls with normal glucose tolerance (NGT), we measured (i) indices of insulin sensitivity of fasting glucose production (by tracer glucose) and glucose disposal (M value on a 240 pmol x min(-1) x m(-2) insulin clamp) and (ii) indices of beta-cell function (glucose sensitivity, rate sensitivity, and potentiation) derived from model analysis (Am J Physiol 283:E1159-E1166, 2002) of the insulin secretory response (by C-peptide deconvolution) to oral glucose. RESULTS: In comparison with NGT, IGT were modestly insulin resistant (M=29+/-2 vs 35+/-2 micromol x min(-1) x kg(FFM)(-1), p=0.01); insulin sensitivity of glucose production also was reduced, in approximate proportion to M. Despite higher baseline insulin secretion rates, IGT was characterized by a 50% reduction in glucose sensitivity [53 (36) vs 102 (123) pmol x min(-1) x m(-2) x mM(-1), median (interquartile range), p=0.001] and impaired potentiation [1.6 (0.8) vs 2.0 (1.5) units, p<0.04] of insulin release, whereas rate sensitivity [1.15 (1.15) vs 1.38 (1.28) nmol x m(-2) x mM(-1)] was not significantly reduced. Glucose sensitivity made the single largest contribution (approximately 50%) to the observed variability of glucose tolerance. CONCLUSION/INTERPRETATION: In IGT the defect in glucose sensitivity of insulin release quantitatively predominates over insulin resistance in the genesis of the reduced tolerance to oral glucose. (literal)

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