<rdf:RDF xmlns:rdf="http://www.openarchives.org/OAI/2.0/rdf/" xmlns:ow="http://www.ontoweb.org/ontology/1#" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:ds="http://dspace.org/ds/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/rdf/ http://www.openarchives.org/OAI/2.0/rdf.xsd">
   <ow:Publication rdf:about="oai:digibug.ugr.es:10481/110739">
      <dc:title>Exogenous leptin reinforces intestinal barrier function and protects from colitis</dc:title>
      <dc:creator>Rivero Gutiérrez, Belén</dc:creator>
      <dc:creator>Aranda Clemente, Carlos José</dc:creator>
      <dc:creator>Ocón, Borja</dc:creator>
      <dc:creator>Arredondo-Amador, María</dc:creator>
      <dc:creator>Martínez Augustín, María Olga</dc:creator>
      <dc:creator>Sánchez De Medina López-Huertas, Fermín</dc:creator>
      <dc:subject>Leptin</dc:subject>
      <dc:subject>Barrier function</dc:subject>
      <dc:subject>Experimental colitis</dc:subject>
      <dc:description>The authors are thankful to Mercedes González and other laboratory members for their assistance, as well as to Dr. Diego Pérez Tilve (University of Cincinnati). This work was supported by the Ministerio de Economía y Competitividad (SAF2011-22922, SAF2011-22812, BFU2014-57736-P, AGL2014-58883-R) and Junta de Andalucía (CTS164, CTS235). BRG, CJA, BO and MAA are funded by Ministry of Education. CIBERehd is funded by the Instituto de Salud Carlos III.</dc:description>
      <dc:description>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.</dc:description>
      <dc:date>2026-02-09T07:37:45Z</dc:date>
      <dc:date>2026-02-09T07:37:45Z</dc:date>
      <dc:date>2019-09</dc:date>
      <dc:type>journal article</dc:type>
      <dc:identifier>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</dc:identifier>
      <dc:identifier>1096-1186</dc:identifier>
      <dc:identifier>1043-6618</dc:identifier>
      <dc:identifier>https://hdl.handle.net/10481/110739</dc:identifier>
      <dc:identifier>10.1016/j.phrs.2019.104356</dc:identifier>
      <dc:language>eng</dc:language>
      <dc:rights>open access</dc:rights>
      <dc:publisher>Elsevier</dc:publisher>
   </ow:Publication>
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