RT Journal Article
T1 Ghrelin mitigates beta-cell mass loss during insulitis in an animal model of autoimmune diabetes mellitus, the BioBreeding/Worcester rat
A1 Baena-Nieto, Gloria
A1 Lomas-Romero, Isabel M.
A1 Mateos, Rosa M.
A1 Leal-Cosme, Noelia
A1 Perez-Arana, Gonzalo
A1 Aguilar-Diosdado, Manuel
A1 Segundo, Carmen
A1 Lechuga-Sancho, Alfonso M.
K1 ghrelin
K1 autoimmne
K1 prevention
K1 beta-cell viability
K1 cytokines
K1 type 1 diabetes
K1 Cytokine gene-expression
K1 Kappa-b activation
K1 Acute-pancreatitis
K1 Unacylated ghrelin
K1 Apoptosis
K1 Islets
K1 Streptozotocin
K1 Differentiation
K1 Inflammation
K1 Endocrine
AB Background 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 (p
PB Wiley
SN 1520-7552
YR 2017
FD 2017-01-01
LK http://hdl.handle.net/10668/18608
UL http://hdl.handle.net/10668/18608
LA en
DS RISalud
RD Apr 17, 2025