VMP1- Related autophagy induced by fructose rich diet in β-cells: its prevention by incretins
| cic.institucionOrigen | Centro de Endocrinología Experimental y Aplicada | es |
| cic.isFulltext | true | es |
| cic.isPeerReviewed | true | es |
| cic.lugarDesarrollo | Centro de Endocrinología Experimental y Aplicada | es |
| cic.lugarDesarrollo | Universidad de Buenos Aires | es |
| cic.version | info:eu-repo/semantics/acceptedVersion | es |
| dc.date.accessioned | 2019-07-12T14:10:53Z | |
| dc.date.available | 2019-07-12T14:10:53Z | |
| dc.identifier.uri | https://digital.cic.gba.gob.ar/handle/11746/10135 | |
| dc.title | VMP1- Related autophagy induced by fructose rich diet in β-cells: its prevention by incretins | en |
| dc.type | Artículo | es |
| dcterms.abstract | To demonstrate the role of autophagy and incretins on fructose‐induced alteration in β‐cell mass and function. Methods: Normal Wistar rats were fed (3 weeks) with commercial diet without (C) or with 10% fructose in drinking water (F) alone or plus sitagliptin (CS and FS) or exendin‐4 (CE and FE). Serum levels of metabolic/endocrine parameters, β‐cell mass, morphology/ultrastructure and apoptosis, VMP1 expression and glucose‐stimulated insulin secretion (GSIS) were studied. Complementary, islets isolated from normal rats were cultured (3 days) without (C) or with F and F plus exendin‐4 (FE) or chloroquine (FCQ). Expression of autophagy related‐proteins (VMP1 and LC3), apoptotic/antiapoptotic markers (caspase‐3 and Bcl‐2), GSIS and insulin mRNA levels were measured. Results: F rats developed impaired glucose tolerance (IGT) and a significant increase in plasma triglyceride, TBARS, insulin levels, HOMAIR and HOMA‐β indexes. Significant β‐cell mass reduction was associated to an increased apoptotic rate and morphological/ultrastructural changes indicative of autophagic activity. All these changes were prevented by either sitagliptin or exendin‐4. In cultured islets, F significantly enhanced insulin mRNA and GSIS, decreased Bcl‐2 mRNA levels and increased caspase‐3 expression. Chloroquine reduced these changes suggesting autophagy participation in this process. Indeed, F induced the increase of both, VMP1 expression and LC3‐II, suggesting that VMP1‐related autophagy is activated in injured β‐cell. Exendin‐4 prevented islet‐cell damage and autophagy development. Conclusions: VMP1‐related autophagy is a reactive process against Finduced islet dysfunction, being prevented by exendin‐4 treatment. This knowledge could help to use autophagy as potential target for preventing progression from IGT toT2DM. | en |
| dcterms.creator.author | Maiztegui, Bárbara | es |
| dcterms.creator.author | Boggio, Verónica | es |
| dcterms.creator.author | Román, Carolina Lisi | es |
| dcterms.creator.author | Flores, Luis Emilio | es |
| dcterms.creator.author | Del Zotto, Héctor | es |
| dcterms.creator.author | Ropolo, Alejandro | es |
| dcterms.creator.author | Grasso, Daniel | es |
| dcterms.creator.author | Vaccaro, María I. | es |
| dcterms.creator.author | Gagliardino, Juan José | es |
| dcterms.extent | 43 p. | es |
| dcterms.identifier.other | doi.10.1042/CS20170010 | es |
| dcterms.identifier.url | Recurso online | es |
| dcterms.isPartOf.issue | vol. 131, no. 8 | es |
| dcterms.isPartOf.series | Clinical Science | es |
| dcterms.issued | 2017-08 | |
| dcterms.language | Inglés | es |
| dcterms.license | Attribution-NonCommercial-ShareAlike 4.0 International (BY-NC-SA 4.0) | es |
| dcterms.subject | incretins | en |
| dcterms.subject | fructose-induced β-cell-injury | en |
| dcterms.subject | autophagy | en |
| dcterms.subject | β-cell mass | en |
| dcterms.subject | β-cell function | en |
| dcterms.subject.materia | Bioquímica y Biología Molecular | es |
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