http://www.cnr.it/ontology/cnr/individuo/prodotto/ID209736
Adenoviral Gene Transfer of PLD1-D4 Enhances Insulin Sensitivity in Mice by Disrupting Phospholipase D1 Interaction with PED/PEA-15. (Articolo in rivista)
- Type
- Label
- Adenoviral Gene Transfer of PLD1-D4 Enhances Insulin Sensitivity in Mice by Disrupting Phospholipase D1 Interaction with PED/PEA-15. (Articolo in rivista) (literal)
- Anno
- 2013-01-01T00:00:00+01:00 (literal)
- Alternative label
Cassese A, Raciti GA, Fiory F, Nigro C, Ulianich L, Castanò I, D'Esposito V, Terracciano D, Pastore L, Formisano P, Beguinot F, Miele C. (2013)
Adenoviral Gene Transfer of PLD1-D4 Enhances Insulin Sensitivity in Mice by Disrupting Phospholipase D1 Interaction with PED/PEA-15.
in PloS one
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Cassese A, Raciti GA, Fiory F, Nigro C, Ulianich L, Castanò I, D'Esposito V, Terracciano D, Pastore L, Formisano P, Beguinot F, Miele C. (literal)
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Dipartimento di Scienze Mediche e Traslazionali, Università di Napoli \"Federico II\" and Istituto di Endocrinologia e Oncologia Sperimentale Gaetano Salvatore, Consiglio Nazionale delle Ricerche, Naples, Italy. (literal)
- Titolo
- Adenoviral Gene Transfer of PLD1-D4 Enhances Insulin Sensitivity in Mice by Disrupting Phospholipase D1 Interaction with PED/PEA-15. (literal)
- Abstract
- Over-expression of phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes (PED/PEA-15) causes insulin resistance by interacting with the D4 domain of phospholipase D1 (PLD1). Indeed, the disruption of this association restores insulin sensitivity in cultured cells over-expressing PED/PEA-15. Whether the displacement of PLD1 from PED/PEA-15 improves insulin sensitivity in vivo has not been explored yet. In this work we show that treatment with a recombinant adenoviral vector containing the human D4 cDNA (Ad-D4) restores normal glucose homeostasis in transgenic mice overexpressing PED/PEA-15 (Tg ped/pea-15) by improving both insulin sensitivity and secretion. In skeletal muscle of these mice, D4 over-expression inhibited PED/PEA-15-PLD1 interaction, decreased Protein Kinase C alpha activation and restored insulin induced Protein Kinase C zeta activation, leading to amelioration of insulin-dependent glucose uptake. Interestingly, Ad-D4 administration improved insulin sensitivity also in high-fat diet treated obese C57Bl/6 mice. We conclude that PED/PEA-15-PLD1 interaction may represent a novel target for interventions aiming at improving glucose tolerance. (literal)
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