2026-06-01T18:07:56Zhttps://riuma.uma.es/rest/oai/requestoai:riuma.uma.es:10630/323122026-02-03T11:36:03Zcom_10630_2254col_10630_37953
LRH-1 agonism favours an immune-islet dialogue which protects against diabetes mellitus
Cobo-Vuilleumier, Nadia
Lorenzo, Petra I
García Rodríguez, Noelia
Herrera Gómez, Irene de Gracia
Fuente-Martin, Esther
López-Noriega, Livia
Mellado-Gil, José Manuel
Romero-Zerbo, Silvana Yanina
Baquié, Mathurin
Lachaud, Christian Claude
Stifter, Katja
Perdomo, German
Bugliani, Marco
De Tata, Vincenzo
Bosco, Domenico
Parnaud, Geraldine
Pozo, David
Hmadcha, Abdelkrim
Florido, Javier P
Toscano, Miguel G
de Haan, Peter
Schoonjans, Kristina
Sánchez Palazón, Luis
Marchetti, Piero
Schirmbeck, Reinhold
Martín-Montalvo, Alejandro
Meda, Paolo
Bernat, Soria
Bermúdez Silva, Francisco Javier
St-Onge, Luc
Gauthier, Benoit R
Hmadcha, Abdelkrim
Diabetes
Type 1 diabetes mellitus (T1DM) is due to the selective destruction of islet beta cells by
immune cells. Current therapies focused on repressing the immune attack or stimulating beta
cell regeneration still have limited clinical efficacy. Therefore, it is timely to identify innovative
targets to dampen the immune process, while promoting beta cell survival and function. Liver
receptor homologue-1 (LRH-1) is a nuclear receptor that represses inflammation in digestive
organs, and protects pancreatic islets against apoptosis. Here, we show that BL001, a small
LRH-1 agonist, impedes hyperglycemia progression and the immune-dependent inflammation
of pancreas in murine models of T1DM, and beta cell apoptosis in islets of type 2 diabetic
patients, while increasing beta cell mass and insulin secretion. Thus, we suggest that LRH-1
agonism favors a dialogue between immune and islet cells, which could be druggable to
protect against diabetes mellitus.
2024-07-25T10:38:05Z
2024-07-25T10:38:05Z
2018
journal article
Cobo-Vuilleumier, N., Lorenzo, P.I., Rodríguez, N.G. et al. LRH-1 agonism favours an immune-islet dialogue which protects against diabetes mellitus. Nat Commun 9, 1488 (2018). https://doi.org/10.1038/s41467-018-03943-0
https://hdl.handle.net/10630/32312
10.1038/s41467-018-03943-0
eng
http://creativecommons.org/licenses/by/4.0/
open access
Atribución 4.0 Internacional
Nature Research