Vildagliptin, a dipeptidyl peptidase-IV inhibitor, improves model-assessed beta-cell function in patients with type 2 diabetes (Articolo in rivista)

Type
Label
  • Vildagliptin, a dipeptidyl peptidase-IV inhibitor, improves model-assessed beta-cell function in patients with type 2 diabetes (Articolo in rivista) (literal)
Anno
  • 2005-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1210/jc.2004-2460 (literal)
Alternative label
  • Mari A.; Sallas W. M.; He Y. L.; Watson C.; Ligueros-Saylan M.; Dunning B. E.; Deacon C. F.; Holst J. J.; Foley J. E. (2005)
    Vildagliptin, a dipeptidyl peptidase-IV inhibitor, improves model-assessed beta-cell function in patients with type 2 diabetes
    in The Journal of clinical endocrinology and metabolism
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Mari A.; Sallas W. M.; He Y. L.; Watson C.; Ligueros-Saylan M.; Dunning B. E.; Deacon C. F.; Holst J. J.; Foley J. E. (literal)
Pagina inizio
  • 4888 (literal)
Pagina fine
  • 4894 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 90 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 8 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1: National Research Center, Institute of Biomedical Engineering, Padova, Italy / 2, 5, 9: Novartis Pharmaceuticals Corp., East Hanover, New Jersey 07936 / 3, 4: Novartis Institutes for Biomedical Research, Cambridge, Massachusetts 02139 / 6: PharmaWrite, LLC (B.E.D.), Princeton, NJ 08540 / 7, 8: Panum Institute, University of Copenhagen, Copenhagen, Denmark (literal)
Titolo
  • Vildagliptin, a dipeptidyl peptidase-IV inhibitor, improves model-assessed beta-cell function in patients with type 2 diabetes (literal)
Abstract
  • vildagliptin, increases levels of intact glucagon-like peptide-1 (GLP-1) and improves glycemic control in patients with type 2 diabetes. Although GLP-1 is known to stimulate insulin secretion, vildagliptin does not affect plasma insulin levels in diabetic patients, suggesting that more sophisticated measures are necessary to ascertain the influence of vildagliptin on ?-cell function. Methods: This study examined the effects of 28-d treatment with vildagliptin (100 mg, twice daily; n ? 9) vs. placebo (n ? 11) on ?-cell function in diabetic patients using a mathematical model that describes the insulin secretory rate as a function of glucose levels (?-cell dose response), the change in glucose with time (derivative component), and a potentiation factor, which is a function of time and may reflect the actions of nonglucose secretagogues and other factors. Results: Vildagliptin significantly increased the insulin secretory rate at 7 mmol/liter glucose (secretory tone), calculated from the dose response; the difference in least squares mean (?LSM) was 101 ? 51 pmol?min?1?m?2 (P?0.002). The slope of the ?-cell dose response, the derivative component, and the potentiation factor were not affected. Vildagliptin also significantly decreased mean prandial glucose (?LSM, ?1.2 ? 0.4 mmol/liter; P ? 0.01) and glucagon (?LSM, ?10.7 ? 4.8 ng/liter; P ? 0.03) levels and increased plasma levels of intact GLP-1 (?LSM, ?10.8 ? 1.6 pmol/liter; P ? 0.0001) and gastric inhibitory polypeptide (?LSM, ?43.4 ? 9.4 pmol/liter; P ? 0.0001) relative to placebo. Conclusion: Vildagliptin is an incretin degradation inhibitor that improves ?-cell function in diabetic patients by increasing the insulin secretory tone (literal)
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