2026-08-19T22:32:54Zhttps://riubu.ubu.es/oai/requestoai:riubu.ubu.es:10259/49932021-11-10T09:38:26Zcom_10259_4725com_10259_5086com_10259_2604col_10259_4726
00925njm 22002777a 4500
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Cobo Vuilleumier, Nadia .
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Lorenzo, Petra Isabel .
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García Rodríguez, Noelia .
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Gracia Herrera-Gómez, Irene de .
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Fuente Martín, Esther .
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López Noriega, Livia
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Mellado Gil, José Manuel .
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Romero Zerbo, Silvana-Yanina .
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Baquié, Mathurin .
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Lachaud, Christian Claude .
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Stifter, Katja .
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Perdomo Hernández, Germán M.
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Bugliani, Marco .
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Tata, Vincenzo de .
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Bosco, Domenico .
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Parnaud, Geraldine .
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Pozo, David .
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Hmadcha, Abdelkrim .
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Florido, Javier P. .
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Toscano, Miguel G. .
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Haan, Peter de .
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Schoonjans, Kristina .
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Sánchez Palazón, Luis .
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Marchetti, Piero .
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Schirmbeck, Reinhold .
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Martín Montalvo, Alejandro .
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Meda, Paolo .
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Soria, Bernat .
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Bermúdez Silva, Francisco Javier .
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St-Onge16, Luc .
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Gauthier, Benoit R. .
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2018-04
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.
2041-1723
http://hdl.handle.net/10259/4993
10.1038/s41467-018-03943-0
LRH-1 agonism favours an immune-islet dialogue which protects against diabetes mellitus