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Ghrelin's effects on proinflammatory cytokine mediated apoptosis and their impact on β-cell functionality

AutorDiaz-Ganete, Antonia; Baena-Nieto, Gloria; Lomas-Romero, Isabel M.; López-Acosta, José Francisco ; Cózar-Castellano, Irene ; Medina, Francisco; Segundo, Carmen; Lechuga-Sancho, Alfonso Maria
Fecha de publicación2015
EditorHindawi Publishing Corporation
CitaciónInternational Journal of Endocrinology 2015: 235727 (2015)
ResumenGhrelin is a peptidic hormone, which stimulates cell proliferation and inhibits apoptosis in several tissues, including pancreas. In preclinical stage of type 1 diabetes, proinflammatory cytokines generate a destructive environment for β-cells known as insulitis, which results in loss of β-cell mass and impaired insulin secretion, leading to diabetes. Our aim was to demonstrate that ghrelin could preserve β-cell viability, turnover rate, and insulin secretion acting as a counter balance of cytokines. In the present work we reproduced proinflammatory milieu found in insulitis stage by treating murine cell line INS-1E and rat islets with a cytokine cocktail including IL-1β, IFNγ, and TNFα and/or ghrelin. Several proteins involved in survival pathways (ERK 1/2 and Akt/PKB) and apoptosis (caspases and Bcl-2 protein family and endoplasmic reticulum stress markers) as well as insulin secretion were analyzed. Our results show that ghrelin alone has no remarkable effects on β-cells in basal conditions, but interestingly it activates cell survival pathways, downregulates apoptotic mediators and endoplasmic reticulum stress, and restores insulin secretion in response to glucose when beta-cells are cytokine-exposed. These data suggest a potential role of ghrelin in preventing or slowing down the transition from a preclinical to clinically established diabetes by ameliorating the effects of insulitis on β-cells.
Versión del editorhttps://doi.org/10.1155/2015/235727
Identificadoresdoi: 10.1155/2015/235727
e-issn: 1687-8345
issn: 1687-8337
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