Pancreatic islet amyloidosis, beta-cell apoptosis, and alpha-cell proliferation are determinants of islet remodeling in type-2 diabetic baboons (Articolo in rivista)

Type
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  • Pancreatic islet amyloidosis, beta-cell apoptosis, and alpha-cell proliferation are determinants of islet remodeling in type-2 diabetic baboons (Articolo in rivista) (literal)
Anno
  • 2009-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1073/pnas.0906471106 (literal)
Alternative label
  • Guardado-Mendoza R, Davalli AM, Chavez AO, Hubbard GB, Dick EJ, Majluf-Cruz A, Tene-Perez CE, Goldschmidt L, Hart J, Perego C, Comuzzie AG, Tejero ME, Finzi G, Placidi C, La Rosa S, Capella C, Halff G, Gastaldelli A, DeFronzo RA, Folli F (2009)
    Pancreatic islet amyloidosis, beta-cell apoptosis, and alpha-cell proliferation are determinants of islet remodeling in type-2 diabetic baboons
    in Proceedings of the National Academy of Sciences of the United States of America; National Academy of Sciences, Washington (Stati Uniti d'America)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Guardado-Mendoza R, Davalli AM, Chavez AO, Hubbard GB, Dick EJ, Majluf-Cruz A, Tene-Perez CE, Goldschmidt L, Hart J, Perego C, Comuzzie AG, Tejero ME, Finzi G, Placidi C, La Rosa S, Capella C, Halff G, Gastaldelli A, DeFronzo RA, Folli F (literal)
Pagina inizio
  • 13992 (literal)
Pagina fine
  • 13997 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
  • http://www.ncbi.nlm.nih.gov/pubmed/19666551 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 106 (literal)
Rivista
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  • 6 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 33 (literal)
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  • PubMe (literal)
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1. Univ Texas Hlth Sci Ctr San Antonio, Diabet Div, Dept Med, San Antonio, TX 78229 USA 2. Ist Sci San Raffaele, I-20132 Milan, Italy 3. SW Fdn Biomed Res, San Antonio, TX 78227 USA 4. SW Natl Primate Res Ctr, San Antonio, TX 78227 USA 5. Unidad Invest Med Trombosis & Aterogenesis, Mexico City, DF, Mexico 6. Univ Colima, Sch Med, Colima 28040, Mexico 7. Univ Calif Los Angeles, Dept Energy, Inst Genom & Proteom, Howard Hughes Med Inst, Los Angeles, CA 90095 USA 8. Univ Texas Hlth Sci Ctr San Antonio, Dept Biochem, San Antonio, TX 78229 USA 9. S Texas Vet Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Audie Murphy Div, Dept Vet Affairs, San Antonio, TX 78229 USA 10. Univ Milan, Dept Mol Sci Appl Biosyst, I-20134 Milan, Italy 11. Univ Insubria, Dept Human Morphol, Osped Circolo, Dept Pathol, I-21100 Varese, Italy 12. Ctr Insubre Biotecnol Salute Umana, I-21100 Varese, Italy 13. Univ Texas Hlth Sci Ctr San Antonio, Dept Surg, San Antonio, TX 78229 USA 14. CNR, Fdn G Monasterio, I-56126 Pisa, Italy 15. CNR, Inst Clin Physiol, I-56126 Pisa, Italy (literal)
Titolo
  • Pancreatic islet amyloidosis, beta-cell apoptosis, and alpha-cell proliferation are determinants of islet remodeling in type-2 diabetic baboons (literal)
Abstract
  • beta-Cell dysfunction is an important factor in the development of hyperglycemia of type-2 diabetes mellitus, and pancreatic islet amyloidosis (IA) has been postulated to be one of the main contributors to impaired insulin secretion. The aim of this study was to evaluate the correlation of IA with metabolic parameters and its effect on islets of Langerhans remodeling and relative endocrine-cell volume in baboons. We sequenced the amylin peptide, determined the fibrillogenic propensities, and evaluated pancreatic histology, clinical and biochemical characteristics, and endocrine cell proliferation and apoptosis in 150 baboons with different metabolic status. Amylin sequence in the baboon was 92% similar to humans and showed superimposable fibrillogenic propensities. IA severity correlated with fasting plasma glucose (FPG) (r = 0.662, P < 0.001) and HbA1c (r = 0.726, P < 0.001), as well as with free fatty acid, glucagon values, decreased homeostasis model assessment (HOMA) insulin resistance, and HOMA-B. IA severity was associated with a decreased relative beta-cell volume, and increased relative alpha-cell volume and hyperglucagonemia. These results strongly support the concept that IA and beta-cell apoptosis in concert with alpha-cell proliferation and hypertrophy are key determinants of islets of Langerhans \"dysfunctional remodeling'' and hyperglycemia in the baboon, a nonhuman primate model of type-2 diabetes mellitus. The most important determinants of IA were age and FPG (R(2) = 0.519, P < 0.0001), and different FPG levels were sensitive and specific to predict IA severity. Finally, a predictive model for islet amyloid severity was generated with age and FPG as required variables. (literal)
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