@prefix prodottidellaricerca: . @prefix istituto: . @prefix prodotto: . istituto:CDS045 prodottidellaricerca:prodotto prodotto:ID285280 . istituto:CDS061 prodottidellaricerca:prodotto prodotto:ID285280 . @prefix pubblicazioni: . @prefix unitaDiPersonaleInterno: . unitaDiPersonaleInterno:MATRICOLA39052 pubblicazioni:autoreCNRDi prodotto:ID285280 . @prefix modulo: . modulo:ID2507 prodottidellaricerca:prodotto prodotto:ID285280 . @prefix rdf: . prodotto:ID285280 rdf:type prodotto:TIPO1101 . @prefix retescientifica: . prodotto:ID285280 rdf:type retescientifica:ProdottoDellaRicerca . @prefix rdfs: . prodotto:ID285280 rdfs:label "Does dipeptidyl peptidase-4 inhibition prevent the diabetogenic effects of glucocorticoids in men with the metabolic syndrome? A randomized controlled trial (Articolo in rivista)"@en . @prefix xsd: . prodotto:ID285280 pubblicazioni:anno "2014-01-01T00:00:00+01:00"^^xsd:gYear ; pubblicazioni:doi "10.1530/EJE-13-0610"^^xsd:string . @prefix skos: . prodotto:ID285280 skos:altLabel "
Van Genugten R.E.; Van Raalte D.H.; Muskiet M.H.; Heymans M.W.; Pouwels P.J.W.; Ouwens D.M.; Mari A.; Diamant M. (2014)
Does dipeptidyl peptidase-4 inhibition prevent the diabetogenic effects of glucocorticoids in men with the metabolic syndrome? A randomized controlled trial
in European journal of endocrinology (Online)
"^^rdf:HTML ; pubblicazioni:autori "Van Genugten R.E.; Van Raalte D.H.; Muskiet M.H.; Heymans M.W.; Pouwels P.J.W.; Ouwens D.M.; Mari A.; Diamant M."^^xsd:string ; pubblicazioni:paginaInizio "429"^^xsd:string ; pubblicazioni:paginaFine "439"^^xsd:string ; pubblicazioni:url "http://www.ncbi.nlm.nih.gov/pubmed/24297090"^^xsd:string ; pubblicazioni:numeroVolume "170"^^xsd:string . @prefix ns11: . prodotto:ID285280 pubblicazioni:rivista ns11:ID194475 ; pubblicazioni:numeroFascicolo "3"^^xsd:string ; skos:note "Scopu"^^xsd:string ; pubblicazioni:affiliazioni "Department of Internal Medicine, Diabetes Center, PO Box 7057, 1007 MB Amsterdam, Netherlands; Department of Methodology and Applied Biostatistics, Institute of Health Sciences, PO Box 7057, 1007 MB Amsterdam, Netherlands; Department of Physics and Medical Technology, VU University Medical Center, PO Box 7057, 1007 MB Amsterdam, Netherlands; Institute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, D\u00FCsseldorf, Germany; Department of Endocrinology, Ghent University Hospital, Ghent, Belgium; Institute of Biomedical Engineering, National Research Council, Padova, Italy"^^xsd:string ; pubblicazioni:titolo "Does dipeptidyl peptidase-4 inhibition prevent the diabetogenic effects of glucocorticoids in men with the metabolic syndrome? A randomized controlled trial"^^xsd:string ; prodottidellaricerca:abstract "Objective: Anti-inflammatory glucocorticoid (GC) therapy often induces hyperglycemia due to insulin resistance and islet-cell dysfunction. Incretin-based therapies may preserve glucose tolerance and pancreatic islet-cell function. In this study, we hypothesized that concomitant administration of the dipeptidyl peptidase-4 inhibitor sitagliptin and prednisolone in men at high risk to develop type 2 diabetes could protect against the GC-induced diabetogenic effects. Design and methods : Men with the metabolic syndrome but without diabetes received prednisolone 30 mg once daily plus sitagliptin 100 mg once daily (n=14), prednisolone (n=12) or sitagliptin alone (n=14) or placebo (n=12) for 14 days in a double-blind 2x2 randomized-controlled study. Glucose, insulin, C-peptide, and glucagon were measured in the fasted state and following a standardized mixed-meal test. ?-cell function parameters were assessed both from a hyperglycemic-arginine clamp procedure and from the meal test. Insulin sensitivity (M-value) was measured by euglycemic clamp. Results: Prednisolone increased postprandial area under the curve (AUC)-glucose by 17% (P<0.001 vs placebo) and postprandial AUC-glucagon by 50% (P<0.001). Prednisolone reduced 1st and 2nd phase glucose-stimulated- and combined hyperglycemia-arginine-stimulated C-peptide secretion (all P<=0.001). When sitagliptin was added, both clamp-measured ?-cell function (P=NS for 1st and 2nd phase vs placebo) and postprandial hyperglucagonemia (P=NS vs placebo) remained unaffected. However, administration of sitagliptin could not prevent prednisolone-induced increment in postprandial glucose concentrations (P<0.001 vs placebo). M-value was not altered by any treatment. Conclusion: Fourteen-day treatment with high-dose prednisolone impaired postprandial glucose metabolism in subjects with the metabolic syndrome. Concomitant treatment with sitagliptin improved various aspects of pancreatic islet-cell function, but did not prevent deterioration of glucose tolerance by GC treatment. \u00A9 2014 European Society of Endocrinology."@en ; prodottidellaricerca:prodottoDi istituto:CDS045 , istituto:CDS061 , modulo:ID2507 ; pubblicazioni:autoreCNR unitaDiPersonaleInterno:MATRICOLA39052 . ns11:ID194475 pubblicazioni:rivistaDi prodotto:ID285280 .