Liraglutide improves surfactant protein-B production and reduces right ventricular hypertrophy in a rat model of intersitial pulmonary fibrosis

Juan Fandino Gomez; Marina Romani Perez; Veronica Outeirino Iglesias; Yolanda Diz Chaves; Maria Gonzalez Nunez; Houcine Dab; Eva MariaVigo Gago; Lucas Gonzalez Matias; Federico Mallo Ferrer

doi:10.1530/endoabs.37.EP620

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Endocrine Abstracts (2015) 37 EP620 | DOI: 10.1530/endoabs.37.EP620

ECE2015 Eposter Presentations Obesity and cardiovascular endocrinology (108 abstracts)

Liraglutide improves surfactant protein-B production and reduces right ventricular hypertrophy in a rat model of intersitial pulmonary fibrosis

Juan Fandiño Gómez ^1, , Marina Romaní Pérez ³ , Verónica Outeiriño Iglesias ^1, , Yolanda Diz Chaves ^1, , María González Núñez ^1, , Houcine Dab ⁴ , Eva MaríaVigo Gago ^1, , Lucas González Matías ^1, & Federico Mallo Ferrer ^1,

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¹Faculty of Biology, University of Vigo, Vigo, Pontevedra, Spain; ²Group of Endocrinology and Neurophysiology, Biomedical Research Center (CINBIO), University of Vigo, Vigo, Pontevedra, Spain; ³Nutrineuro, University of Bordeaux, INRA, Bordeaux, Aquitaine, France; ⁴Higher Institute of Applied Biology Medenine (ISBAM), University of Gabes, Medenine, Tunisia.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and fatal lung disease characterized by excessive matrix deposition that disrupts the normal alveolar architecture and lung physiology. Glucagon-like peptide 1 (GLP1) is a gut-produced hormone with insulinotropic effects. GLP1 receptor is expressed in the lung where it is implicated in the synthesis of the protein (SPs) and lipid fractions of the surfactant. We have previously shown that the GLP1 receptor agonist, liraglutide (LIR), is able to restore surfactant protein-B (SP-B, a limiting factor for survival) production and right ventricular hypertrophy in streptozotocin-diabetic rats. The aim of this work was to study the effects of the GLP-1 receptor agonist liraglutide in the production of SPs, fibrosis indicators and right ventricle mass in a rat model of IPF. IPF was induced in rats by the single intra-tracheal instillation of bleomycin (BLM, 2.5 mg/kg). From day 10 rats were treated with liraglutide (100 μg/kg per 12 h s.c.), once overwhelmed the acute inflammatory phase, and then they were sacrificed in day 21. Heart ventricles and lungs were isolated, weighted, and frozen. The expression levels of SP-B, thyroid transcription factor 1 (TTF1, a transcription factor for SP-B) and receptors for GLP1 and leptin were lower in lungs of BLM-treated rats; but their levels were restored by liraglutide treatment. The right ventricle weight was also augmented in BLM-treated rats and liraglutide administration partially restored right ventricle masses. We have also measured the expression levels of lung fibrosis indicators as collagen type-IαI and connective tissue growth factor (CTGF), which yielded higher levels in BLM-treated animals, but liraglutide did not modified those. In conclusion, we found that liraglutide was able to increasing pulmonary SP-B and partially reverse right ventricular hypertrophy associated to the lung fibrosis induced by BLM, however, it can’t improve the interstitial fibrosis once consolidated.