PED/PEA-15 regulates glucose-induced insulin secretion by restraining potassium channel expression in pancreatic beta-cells. (Articolo in rivista)

Type

• Articolo in rivista (Classe)
• Prodotto della ricerca (Classe)

Label

• PED/PEA-15 regulates glucose-induced insulin secretion by restraining potassium channel expression in pancreatic beta-cells. (Articolo in rivista) (literal)

Anno

• 2007-01-01T00:00:00+01:00 (literal)

Alternative label

• Miele C; Raciti GA; Cassese A; Romano C; Giacco F; Oriente F; Paturzo F; Andreozzi F; Zabatta A; Troncone G; Bosch F; Pujol A; Chneiweiss H; Formisano P;Beguinot F. (2007)
  PED/PEA-15 regulates glucose-induced insulin secretion by restraining potassium channel expression in pancreatic beta-cells.
  in Diabetes (N.Y.N.Y.)
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Miele C; Raciti GA; Cassese A; Romano C; Giacco F; Oriente F; Paturzo F; Andreozzi F; Zabatta A; Troncone G; Bosch F; Pujol A; Chneiweiss H; Formisano P;Beguinot F. (literal)

Rivista

• Diabetes (Rivista)

Note

• ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• Department of Cellular and Molecular Biology and Pathology and Institute of Experimental Endocrinology and Oncology--CNR, \"Federico II\" University of Naples, Naples, Italy; Department of Clinical and Experimental Medicine, University of Catanzaro \"Magna Graecia,\" Catanzaro, Italy; Department of Biomorphological and Functional Sciences, \"Federico II\" University of Naples, Naples, Italy; Center for Animal Biotechnology and Gene Therapy and Department of Biochemistry and Molecular Biology, School of Veterinary Medicine, Autonomous University of Barcelona, Barcelona, Spain; and INSERM U752, University Paris 5 Rene´ Descartes, Paris, France. (literal)

Titolo

• PED/PEA-15 regulates glucose-induced insulin secretion by restraining potassium channel expression in pancreatic beta-cells. (literal)

Abstract

• The phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes (ped/pea-15) gene is overexpressed in human diabetes and causes this abnormality in mice. Transgenic mice with beta-cell-specific overexpression of ped/pea-15 (beta-tg) exhibited decreased glucose tolerance but were not insulin resistant. However, they showed impaired insulin response to hyperglycemia. Islets from the beta-tg also exhibited little response to glucose. mRNAs encoding the Sur1 and Kir6.2 potassium channel subunits and their upstream regulator Foxa2 were specifically reduced in these islets. Overexpression of PED/PEA-15 inhibited the induction of the atypical protein kinase C (PKC)-zeta by glucose in mouse islets and in beta-cells of the MIN-6 and INS-1 lines. Rescue of PKC-zeta activity elicited recovery of the expression of the Sur1, Kir6.2, and Foxa2 genes and of glucose-induced insulin secretion in PED/PEA-15-overexpressing beta-cells. Islets from ped/pea-15-null mice exhibited a twofold increased activation of PKC-zeta by glucose; increased abundance of the Sur1, Kir6.2, and Foxa2 mRNAs; and enhanced glucose effect on insulin secretion. In conclusion, PED/PEA-15 is an endogenous regulator of glucose-induced insulin secretion, which restrains potassium channel expression in pancreatic beta-cells. Overexpression of PED/PEA-15 dysregulates beta-cell. function and is sufficient to impair glucose tolerance in mice. (literal)

Prodotto di

• Istituto per l'endocrinologia e l'oncologia \"Gaetano Salvatore\" (IEOS) (Istituto)
• Studio dell'espressione e della funzione di geni e proteine coinvolte nel diabete di tipo 2 (SV.P16.001.002) (Modulo)

Autore CNR

• CLAUDIA MIELE (Persona)
• PIETRO FORMISANO (Persona)
• GREGORY ALEXANDER RACITI (Unità di personale interno)
• FRANCESCO BEGUINOT (Unità di personale esterno)

Incoming links:

Autore CNR di

• FRANCESCO BEGUINOT (Unità di personale esterno)
• CLAUDIA MIELE (Persona)
• PIETRO FORMISANO (Persona)
• GREGORY ALEXANDER RACITI (Unità di personale interno)

Prodotto

• Istituto per l'endocrinologia e l'oncologia \"Gaetano Salvatore\" (IEOS) (Istituto)
• Studio dell'espressione e della funzione di geni e proteine coinvolte nel diabete di tipo 2 (SV.P16.001.002) (Modulo)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Diabetes (Rivista)