Exogenous leptin reinforces intestinal barrier function and protects from colitis
Metadatos
Mostrar el registro completo del ítemAutor
Rivero Gutiérrez, Belén; Aranda Clemente, Carlos José; Ocón, Borja; Arredondo-Amador, María; Martínez Augustín, María Olga; Sánchez De Medina López-Huertas, FermínEditorial
Elsevier
Materia
Leptin Barrier function Experimental colitis
Fecha
2019-09Referencia bibliográfica
Published version: Rivero-Gutiérrez B, Aranda CJ, Ocón B, Arredondo M, Martínez-Augustin O, Sánchez de Medina F. Exogenous leptin reinforces intestinal barrier function and protects from colitis. Pharmacol Res. 2019 Sep;147:104356. doi: 10.1016/j.phrs.2019.104356
Patrocinador
Ministerio de Economía y Competitividad (SAF2011-22922, SAF2011-22812, BFU2014-57736-P, AGL2014-58883-R); Junta de Andalucía (CTS164, CTS235); Ministerio de Educación; Instituto de Salud Carlos IIIResumen
Besides its function controlling energy expenditure and food intake, leptin is an important modulator of inflammatory responses. The role of leptin in intestinal inflammation remains controversial, since both pro-inflammatory and anti-inflammatory effects have been reported. This study was carried out to further understand leptin contribution in the inflamed intestinal mucosa. Exogenous PEG-leptin or saline solution was given to C57BL/6 mice for two weeks. After 1 week, acute colitis was induced to C57BL/6 mice using dextran sulfate sodium (DSS) in drinking water. The severity of colitis, inflammatory parameters and mucosal barrier function were evaluated. Overall our results indicate that colitis was less severe in mice receiving leptin, as shown by a decrease in rectal bleeding, epithelial damage and colon inflammatory markers, and improved diarrhea. Leptin-treated mice displayed an increase in the expression of tight junction proteins and proliferative expression markers in colon, indicating a reinforcement in the mucosal barrier function induced by leptin administration. PEG-leptin treatment conferred protection to mice in the DSS model of colitis by reinforcing mucosal barrier function.




