Endocrine Abstracts

Acute lung injury (ALI) is characterized by endothelial and epithelial damage, followed by inflammatory. Glucagon-like peptide-1 (GLP-1) is a gut-produced hormone with insulinotropic effects. GLP-1 receptor is expressed in the lung, and there implicated in the synthesis of surfactant proteins. We have previously shown that liraglutide (LIR), a GLP-1 receptor agonist, restores surfactant protein-B (SPB) levels, a limiting factor for survival, and also angiotensin converting enzymes (ACE and ACE-2), in a type-1 diabetes animal model. The aim of this work was to elucidate the effect of LIR in the production of surfactant proteins and ACEs in an animal model of ALI.

ALI was induced by a single intra-tracheal instillation of bleomycin (BLM, 2.5 mg/kg) on day 0 into rats. Rats were treated with liraglutide (100 μg/kg per 12 h sc.) or vehicle (0.9% saline) from day −1 to day 6, and sacrificed in day 7. Left lungs were extracted & weighted, and caudal lobes used for mRNA extraction.

BLM instillation increases left lung weight, revealing an inflammatory response with interstitial oedema. LIR treatment did not revert lung weight increase, since not attenuating inflammatory process. In agreement, BLM instillation decreases mRNA expression of surfactant proteins A and B (79%, P=0.021 and 72%, P=0.002 vs control group, respectively), which was prevented by the administration of LIR. ACE and ACE-2 expression levels were also markedly reduced after BLM instillation (68%, P<0.01 and 70%, P<0.001 vs control, respectively). Again, LIR administration restored the levels of both enzymes.

In conclusion, LIR restores surfactant proteins and angiotensin converting enzymes expression in the lung, in a rat model of ALI. This implicates that LIR could improve pulmonary functionality in ALI, regardless of the inflammatory response.