Baena-Nieto, GloriaLomas-Romero, Isabel M.Mateos, Rosa M.Leal-Cosme, NoeliaPerez-Arana, GonzaloAguilar-Diosdado, ManuelSegundo, CarmenLechuga-Sancho, Alfonso M.2023-02-092023-02-092017-01-011520-7552http://hdl.handle.net/10668/18608Background Ghrelin is a peptide hormone with pleiotropic effects. It stimulates cell proliferation and inhibits apoptosis-mediated cell death. It prevents diabetes mellitus in several models of chemical, surgical and biological toxic insults to pancreas in both in vivo and in vitro models and promotes glucose-stimulated insulin secretion under cytotoxic conditions. It has not yet been tested in vivo in an autoimmune model of diabetes with a persistent insult to the beta-cell. Given the immunomodulating effects of ghrelin and its trophic effects on beta-cells, we hypothesized that ghrelin treatment during the early stages of insulitis would delay diabetes onset.Methods BioBreeding/Worcester male rats received ghrelin (10 ng/kg/day) before insulitis development. Glucose metabolism was characterized by glucose and insulin tolerance tests. beta-cell mass, islet area, islet number, beta-cell clusters, proliferation and apoptosis and degree of insulitis were analysed by histomorphometry. A Kaplan-Meier survival curve was plotted and analysed applying the log-rank (Mantel-Cox) test.Results Ghrelin treatment significantly reduced the probability of developing diabetes in our model (penghrelinautoimmnepreventionbeta-cell viabilitycytokinestype 1 diabetesCytokine gene-expressionKappa-b activationAcute-pancreatitisUnacylated ghrelinApoptosisIsletsStreptozotocinDifferentiationInflammationEndocrineresearch articleopen access10.1002/dmrr.28131520-7560https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/dmrr.2813397102800001