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Liraglutide Improves Forced Vital Capacity in Individuals With Type 2 Diabetes: Data From the Randomized Cross-Over LIRALUNG Study

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posted on 04.11.2021, 15:14 by Carolina López-Cano, Andreea Ciudin, Enric Sánchez, Francisco Tinahones, Ferran Barbé, Mireia Dalmases, Marta García-Ramírez, Alfonso Soto, Anna Michaela Gaeta, Silvia Pellitero, Raquel Martí, Cristina Hernández, Rafael Simó, Albert Lecube
To evaluate the effect of liraglutide, a glucagon-like peptide 1 receptor agonist, on pulmonary function and serum levels of surfactant protein D (SP-D) in type 2 diabetes. A double-blind, randomized, crossover, placebo-controlled clinical trial comprising 76 patients with a baseline forced expiratory volume in first second <90% of predicted. Liraglutide was administered for 7 weeks (2 weeks of titration plus 5 weeks at 1.8 mg daily). This short duration was intentional to minimize weight loss as a potential confounding factor. Serum level of SP-D was used as a biomarker of alveolar-capillary barrier integrity. Liraglutide exerted a positive impact on forced vital capacity (FVC) in comparison with placebo [ΔFVC: 5.2% of predicted (0.8 to 9.6); p=0.009]. No differences in the other pulmonary variables were observed. Participants under liraglutide treatment also experienced a decrease in serum SP-D (p=0.038). The absolute change in FVC correlated with final serum SP-D in participants receiving liraglutide (r=-0.313, p=0.036). Stepwise multivariate regression analysis showed that final serum SP-D independently predicted changes in FVC. In conclusion, liraglutide increased FVC in patients with type 2 diabetes. This effect was associated with a significant decrease of circulating SP-D, thus pointing to a beneficial effect in the alveolar-capillary function.

Funding

This study was supported by a grant from Novo Nordisk S.A. (Investigator Sponsored Study). CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) and CIBER de Fisiopatología de la Obesidad y Nutrición (CIBEROBN) are initiatives of the Instituto Carlos III.

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