@prefix prodottidellaricerca: . @prefix istituto: . @prefix prodotto: . istituto:CDS045 prodottidellaricerca:prodotto prodotto:ID30512 . @prefix pubblicazioni: . @prefix unitaDiPersonaleInterno: . unitaDiPersonaleInterno:MATRICOLA39052 pubblicazioni:autoreCNRDi prodotto:ID30512 . unitaDiPersonaleInterno:MATRICOLA6729 pubblicazioni:autoreCNRDi prodotto:ID30512 . @prefix modulo: . modulo:ID2507 prodottidellaricerca:prodotto prodotto:ID30512 . @prefix rdf: . prodotto:ID30512 rdf:type prodotto:TIPO1101 . @prefix retescientifica: . prodotto:ID30512 rdf:type retescientifica:ProdottoDellaRicerca . @prefix rdfs: . prodotto:ID30512 rdfs:label "Impaired beta cell glucose sensitivity rather than inadequate compensation for insulin resistance is the dominant defect in glucose intolerance (Articolo in rivista)"@en . @prefix xsd: . prodotto:ID30512 pubblicazioni:anno "2010-01-01T00:00:00+01:00"^^xsd:gYear ; pubblicazioni:doi "10.1007/s00125-009-1647-6"^^xsd:string . @prefix skos: . prodotto:ID30512 skos:altLabel "
Mari A.; Tura A.; Natali A.; Laville M.; Laakso M.; Gabriel R.; Beck-Nielsen H.; Ferrannini E. (2010)
Impaired beta cell glucose sensitivity rather than inadequate compensation for insulin resistance is the dominant defect in glucose intolerance
in Diabetologia (Berl.)
"^^rdf:HTML ; pubblicazioni:autori "Mari A.; Tura A.; Natali A.; Laville M.; Laakso M.; Gabriel R.; Beck-Nielsen H.; Ferrannini E."^^xsd:string ; pubblicazioni:paginaInizio "749"^^xsd:string ; pubblicazioni:paginaFine "756"^^xsd:string ; pubblicazioni:numeroVolume "53"^^xsd:string . @prefix ns11: . prodotto:ID30512 pubblicazioni:rivista ns11:ID393682 ; skos:note "ISI Web of Science (WOS)"^^xsd:string ; pubblicazioni:affiliazioni "1, 2: ISIB-CNR, Corso Stati Uniti 4, 35127 Padua, Italy\n3, 8: Department of Internal Medicine and C.N.R. Institute of Clinical, Physiology, University of Pisa School of Medicine, Pisa, Italy\n4: CRNHRA, Lyon 1 University, Hospices Civils de Lyon, Lyon, France\n5: Department of Medicine, University of Kuopio, Kuopio, Finland\n6: Unidad de Investigacion, Hospital Universitario La Paz, Madrid, Spain\n7: Department of Endocrinology M, Odense University Hospital, Odense, Denmark"^^xsd:string ; pubblicazioni:titolo "Impaired beta cell glucose sensitivity rather than inadequate compensation for insulin resistance is the dominant defect in glucose intolerance"^^xsd:string ; prodottidellaricerca:abstract "Aims/hypothesis It is commonly thought that hyperglycaemia\nresults from insufficient compensation of insulin secretion for\ninsulin resistance. To verify this hypothesis, we assessed beta\ncell function and insulin sensitivity (IS) in a large cohort of\nvolunteers with normal glucose tolerance (NGT) or impaired\nglucose regulation (IGR), i.e. impaired glucose tolerance or\nimpaired fasting glucose.\nMethods In men and women with NGT (n=1,123) or IGR\n(n=156) (age 44\u00B18 years, BMI 25\u00B14 kg/m2, mean \u00B1 SD)\nwe measured: (1) IS by clamp; (2) insulin secretion rates\n(ISR) and beta cell glucose sensitivity (=slope of the insulin\nsecretion/plasma glucose dose-response) by C-peptide\ndeconvolution and OGTT modelling; and (3) acute insulin\nresponse to intravenous glucose.\nResults After controlling for centre, sex, age and BMI, fasting\nand total ISR were inversely related to IS in both groups,\nwhereas beta cell glucose sensitivity was not. Acute insulin\nresponse was reciprocally related to IS in both groups, but the\nrelationships were incompatible with inadequate compensation\nand significance was lost after controlling for fasting ISR. In\nIGR vs NGT, IS was impaired (92 [75] vs 133 [86] ?mol min-1\n[kg fat-free mass]-1 [nmol/l]-1, median [interquartile range],\np<0.0001) as was beta cell glucose sensitivity (69 [46] vs 119\n[83] pmol min-1 m-2 [nmol/l]-1, p<0.0001), whereas fasting\nand total ISR were increased (35% and 25%, respectively, p<\n0.0001). In fully adjusted models, beta cell glucose sensitivity\nwas the strongest determinant of OGTT glucose levels.\nConclusions/interpretation Insulin resistance normally upregulates\nthe secretory tone, with no evidence of defective\ncompensation in IGR. In contrast, beta cell glucose sensitivity\nis independent of insulin resistance, but a key determinant of\nglucose tolerance. This suggests that hyperglycaemia results\nfrom an intrinsic beta cell defect rather than from inadequate\ncompensation for insulin resistance"@en ; prodottidellaricerca:prodottoDi istituto:CDS045 , modulo:ID2507 ; pubblicazioni:autoreCNR unitaDiPersonaleInterno:MATRICOLA6729 , unitaDiPersonaleInterno:MATRICOLA39052 . ns11:ID393682 pubblicazioni:rivistaDi prodotto:ID30512 .