Early metabolic markers of the development of dysglycemia and type 2 diabetes and their physiological significance (Articolo in rivista)

Type
Label
  • Early metabolic markers of the development of dysglycemia and type 2 diabetes and their physiological significance (Articolo in rivista) (literal)
Anno
  • 2013-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.2337/db12-0707 (literal)
Alternative label
  • Ferrannini, E.;Natali, A.;Camastra, S.;Nannipieri, M.;Mari, A.;Adam, K.P.;Milburn, M.V.;Kastenmuller, G.;Adamski, J.;Tuomi, T.;Lyssenko, V.;Groop, L.;Gall, W.E. (2013)
    Early metabolic markers of the development of dysglycemia and type 2 diabetes and their physiological significance
    in Diabetes (N.Y.N.Y.)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Ferrannini, E.;Natali, A.;Camastra, S.;Nannipieri, M.;Mari, A.;Adam, K.P.;Milburn, M.V.;Kastenmuller, G.;Adamski, J.;Tuomi, T.;Lyssenko, V.;Groop, L.;Gall, W.E. (literal)
Pagina inizio
  • 130 (literal)
Pagina fine
  • 137 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
  • http://www.ncbi.nlm.nih.gov/pubmed/23160532 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 62 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 5 (literal)
Note
  • ISI Web of Science (WOS) (literal)
  • Scopu (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1, 2, 3, 4: Department of Internal Medicine, University of Pisa School of Medicine, Pisa, Italy; 5: National Research Council Institute of Biomedical Engineering, Padua, Italy; 6, 7, 13: Metabolon, Inc., Durham, North Carolina; 8: Institute of Bioinformatics and Systems Biology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany; 9: Institute of Experimental Genetics, Genome Analysis Center, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany; 10: Department of Medicine, Helsinki University Central Hospital, and Research Program of Molecular Medicine, University of Helsinki, Helsinki, Finland; the Folkhalsan Research Centre, Helsinki, Finland; 11, 12: Department of Clinical Sciences, Diabetes and Endocrinology, Lund University, Malmö, Sweden (literal)
Titolo
  • Early metabolic markers of the development of dysglycemia and type 2 diabetes and their physiological significance (literal)
Abstract
  • Metabolomic screening of fasting plasma from nondiabetic subjects identified alpha-hydroxybutyrate (alpha-HB) and linoleoyl-glycerophosphocholine (L-GPC) as joint markers of insulin resistance (IR) and glucose intolerance. To test the predictivity of alpha-HB and L-GPC for incident dysglycemia, alpha-HB and L-GPC measurements were obtained in two observational cohorts, comprising 1,261 nondiabetic participants from the Relationship between Insulin Sensitivity and Cardiovascular Disease (RISC) study and 2,580 from the Botnia Prospective Study, with 3-year and 9.5-year follow-up data, respectively. In both cohorts, alpha-HB was a positive correlate and L-GPC a negative correlate of insulin sensitivity, with alpha-HB reciprocally related to indices of beta-cell function derived from the oral glucose tolerance test (OGTT). In follow-up, alpha-HB was a positive predictor (adjusted odds ratios 1.25 [95% CI 1.00-1.60] and 1.26 [1.07-1.48], respectively, for each standard deviation of predictor), and L-GPC was a negative predictor (0.64 [0.48-0.85] and 0.67 [0.54-0.84]) of dysglycemia (RISC) or type 2 diabetes (Botnia), independent of familial diabetes, sex, age, BMI, and fasting glucose. Corresponding area under the receiver operating characteristic curves were 0.791 (RISC) and 0.783 (Botnia), similar in accuracy when substituting alpha-HB and L-GPC with 2-h OGTT glucose concentrations. When their activity was examined, alpha-HB inhibited and L-GPC stimulated glucose-induced insulin release in INS-1e cells. alpha-HB and L-GPC are independent predictors of worsening glucose tolerance, physiologically consistent with a joint signature of IR and beta-cell dysfunction. (literal)
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