Type 2 diabetes (T2DM) is related to reduced pulmonary function. As experimental studies with glucagon-like peptide 1 (GLP-1) have shown an increase in pulmonary surfactant secretion, and the GLP-1 receptor has been found in significant amounts in the lung, it could be hypothesized that the treatment with liraglutide (a GL-1 agonist) will improve this reduced pulmonary function

There is growing evidence to suggest an association between type 2 diabetes and impaired pulmonary function. In this regard, several cross-sectional studies have appeared showing decreased indices of forced expiration, lung volume and diffusion capacity as the main lung dysfunctions detected in type 2 diabetic populations. In fact, diabetes is frequently co-morbid with chronic obstructive pulmonary disease, and data from the Atherosclerosis Risk in Communities Study showed a faster pulmonary function decline in type 2 diabetic patients than in other participants. This is important because the reduction of FEV1 has been demonstrated an independent cause of mortality in diabetic patients.

Interestingly, lung function measures start to decrease several years before the diagnosis of diabetes. In this regard an investigation found that insulin resistance is an independent determinant of pulmonary function in non-diabetic morbidly obese women. In addition, the results suggest that the metabolic pathways related to insulin resistance are crucial in initiating lung abnormalities in type 2 diabetic patients.

The reasons for the association between respiratory disease and diabetes are unclear. However, the relationship between type 2 diabetes and muscle strength, the impairment in lung elastic properties, and the presence of a low-grade chronic inflammation state are involved. In supporting these findings, thickening of the alveolar epithelia and pulmonary capillary basal lamina, fibrosis, centrilobular emphysema, and pulmonary microangiopathy have been detected in autopsies of diabetic patients. In addition, defects in the bronchiolar surfactant layer, which is involved in maintaining airway stability and diameter, may also be considered a contributing factor to the impairment of airway calibre regulation in diabetic patients. When the alveolocapillary barrier is damaged, surfactant proteins leak into the bloodstream. A recent population-based random sample study has described how increased circulating levels of surfactant protein A, the major surfactant-associated protein, were associated with altered glucose tolerance and insulin resistance. Therefore, surfactant defects in diabetic individuals may also lead to an increase in airway resistance and to a reduction in ventilatory patterns as observed in our studies. In addition, as experimental studies have shown that glucagon-like peptide 1 plays a role in the stimulation of surfactant production, its underlying deficit in type 2 diabetes could also enhance the airway resistance observed in these patients. However, the beneficial effects on pulmonary function using incretin-based therapies remain to be elucidated.

Clinical trial study hypothesis is that treatment with an incretin mimetic such as liraglutide may ameliorate lung function parameters in type 2 diabetics patients, independently of weight reduction. This hypothesis is based on the following factors:

1. - There is growing evidence to suggest an association between type 2 diabetes and impaired pulmonary function.
2. - In patients with type 2 diabetes, the incretin effect is severely reduced or absent, contributing to the reduced lung function parameters observed in type 2 diabetic patients.
3. - GLP-1 stimulates surfactant production in "in vitro" studies and, in consequence, the increase in surfactant production induced by liraglutide could be the main factor involved in the respiratory improvement.

Inclusion Criteria:

• Signed informed consent.
• Subjects between 40 and 65 years old. Diagnosis of type 2 diabetes mellitus with more than 5 years of evolution of disease.
• Metformin (alone or in combination with sulfonylurea and / or insulin and / or thiazolidinediones) at a stable dose for at least the past 3 months.
• HbA1c ≥ 7,0 y ≤ 9,0 %.
• BMI between 30 and 40 kg / m2.
• No pulmonary disease (COPD, asthma, fibrosis, etc) known.
• Baseline FEV1 decline of equal or greater than 10% in the percentage of the theoretical value.
• Chest radiography without significant changes in the lung parenchyma

Exclusion Criteria:

• Type 1 diabetes mellitus
• Treatment with inhibitors of dipeptidyl peptidase 4 glitazones and / or
• SGLT2 inhibitors.
• Active and former smokers for less than five years ago smoking.
• Chronic obstructive pulmonary disease.
• Respiratory sleep disorders that require treatment with continuous positive pressure in the airway.
• Asthma treatment with bronchodilators.
• Previous bariatric surgery.
• Cardiovascular disease, heart failure and / or stroke.
• Pathology of the chest wall.
• Serum creatinine> 1.7 mg / dl.
• Abnormal results in liver function test (Alanine transaminase/ Aspartate Aminotransferase greater than twice the upper limit of normal).
• History of acute or chronic pancreatitis.
• Personal or family history of medullary thyroid cancer or Multiple
• Endocrine Neoplasia (MEN ) type 2.
• Active neoplasms or neoplastic patients considered disease-free history from less than 5 years ago.
• Women of childbearing age who are pregnant (positive pregnancy test within 14 days before the start of treatment) or intend to get pregnant.
• Lactating women.
• Women of childbearing potential not using adequate contraception (such as oral contraceptives, intrauterine device or barrier method of birth control along with spermicide or surgical sterilization) or unwilling to use during the study (as required by local laws or practices).

7 weeks of treatment.