Progression to diabetes in relatives of type 1 diabetic patients: mechanisms and mode of onset (Articolo in rivista)

Type
Label
  • Progression to diabetes in relatives of type 1 diabetic patients: mechanisms and mode of onset (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.2337/db09-1378 (literal)
Alternative label
  • 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.)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Ferrannini E.; Mari A.; Nofrate V.; Sosenko J. M.; Skyler, J. S. (literal)
Pagina inizio
  • 679 (literal)
Pagina fine
  • 685 (literal)
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  • 59 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 3 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1: Department of Medicine, University of Pisa School of Medicine, Pisa, Italy/ 2, 3: C.N.R. Institute of Biomedical Engineering, Padua, Italy; 4, 5: Division of Endocrinology, University of Miami, Miami, Florida. (literal)
Titolo
  • Progression to diabetes in relatives of type 1 diabetic patients: mechanisms and mode of onset (literal)
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. (literal)
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