@prefix prodottidellaricerca: . @prefix istituto: . @prefix prodotto: . istituto:CDS045 prodottidellaricerca:prodotto prodotto:ID30509 . @prefix pubblicazioni: . @prefix unitaDiPersonaleInterno: . unitaDiPersonaleInterno:MATRICOLA39052 pubblicazioni:autoreCNRDi prodotto:ID30509 . @prefix modulo: . modulo:ID2507 prodottidellaricerca:prodotto prodotto:ID30509 . @prefix rdf: . @prefix retescientifica: . prodotto:ID30509 rdf:type retescientifica:ProdottoDellaRicerca , prodotto:TIPO1101 . @prefix rdfs: . prodotto:ID30509 rdfs:label "Progression to diabetes in relatives of type 1 diabetic patients: mechanisms and mode of onset (Articolo in rivista)"@en . @prefix xsd: . prodotto:ID30509 pubblicazioni:anno "2010-01-01T00:00:00+01:00"^^xsd:gYear ; pubblicazioni:doi "10.2337/db09-1378"^^xsd:string . @prefix skos: . prodotto:ID30509 skos:altLabel "
Ferrannini E.; Mari A.; Nofrate V.; Sosenko J. M.; Skyler, J. S. (2010)
Progression to diabetes in relatives of type 1 diabetic patients: mechanisms and mode of onset
in Diabetes (N.Y.N.Y.)
"^^rdf:HTML ; pubblicazioni:autori "Ferrannini E.; Mari A.; Nofrate V.; Sosenko J. M.; Skyler, J. S."^^xsd:string ; pubblicazioni:paginaInizio "679"^^xsd:string ; pubblicazioni:paginaFine "685"^^xsd:string ; pubblicazioni:numeroVolume "59"^^xsd:string . @prefix ns11: . prodotto:ID30509 pubblicazioni:rivista ns11:ID293517 ; pubblicazioni:numeroFascicolo "3"^^xsd:string ; skos:note "ISI Web of Science (WOS)"^^xsd:string ; pubblicazioni:affiliazioni "1: Department of Medicine, University of Pisa School of Medicine, Pisa, Italy/\n2, 3: C.N.R. Institute of Biomedical Engineering, Padua, Italy;\n4, 5: Division of Endocrinology, University of Miami, Miami, Florida."^^xsd:string ; pubblicazioni:titolo "Progression to diabetes in relatives of type 1 diabetic patients: mechanisms and mode of onset"^^xsd:string ; prodottidellaricerca:abstract "OBJECTIVE: Relatives of type 1 diabetic patients are at enhanced risk of developing diabetes. We investigated the mode of onset of hyperglycemia and how insulin sensitivity and beta-cell function contribute to the progression to the disease. RESEARCH DESIGN AND METHODS: In 328 islet cell autoantibody-positive, nondiabetic relatives from the observational arms of the Diabetes Prevention Trial-1 Study (median age 11 years [interquartile range 8], sequential OGTTs (2,143 in total) were performed at baseline, every 6 months, and 2.7 years [2.7] later, when 115 subjects became diabetic. Beta-cell glucose sensitivity (slope of the insulin-secretion/plasma glucose dose-response function) and insulin sensitivity were obtained by mathematical modeling of the OGTT glucose/C-peptide responses. RESULTS: In progressors, baseline insulin sensitivity, fasting insulin secretion, and total postglucose insulin output were similar to those of nonprogressors, whereas beta-cell glucose sensitivity was impaired (median 48 pmol/min per m2 per mmol/l [interquartile range 36] vs. 87 pmol/min per m2 per mmol/l [67]; P < 0.0001) and predicted incident diabetes (P < 0.0001) independently of sex, age, BMI, and clinical risk. In progressors, 2-h glucose levels changed little until 0.78 years before diagnosis, when they started to rise rapidly (approximately 13 mmol x l(-1) x year(-1)); glucose sensitivity began to decline significantly (P < 0.0001) earlier (1.45 years before diagnosis) than the plasma glucose surge. During this anticipation phase, both insulin secretion and insulin sensitivity were essentially stable. CONCLUSIONS: In high-risk relatives, beta-cell glucose sensitivity is impaired and is a strong predictor of diabetes progression. The time trajectories of plasma glucose are frequently biphasic, with a slow linear increase followed by a rapid surge, and are anticipated by a further deterioration of beta-cell glucose sensitivity."@en ; prodottidellaricerca:prodottoDi modulo:ID2507 , istituto:CDS045 ; pubblicazioni:autoreCNR unitaDiPersonaleInterno:MATRICOLA39052 . ns11:ID293517 pubblicazioni:rivistaDi prodotto:ID30509 .