A possible association between fructose consumption and pulmonary emphysema

Camila Liyoko Suehiro,Clarice Rosa Olivo,Alessandra Choqueta De Toledo-Arruda,Milton De Arruda Martins,Chin Jia Lin,Rodolfo De Paula Vieira,Francine Maria De Almeida

doi:10.1038/s41598-019-45594-1

Abstract

Chronic Obstructive Pulmonary Disease (COPD) is a syndrome that comprises several distinct and overlapping phenotypes. In addition to persistent airflow limitation and respiratory symptoms, COPD is also characterized by chronic systemic inflammation. Epidemiological studies have shown that dietary fibers, fruits and vegetables intake protects against the COPD development, while fructose-loading is associated with increased risk of asthma and chronic bronchitis. Since dietary factors might affect susceptibility to COPD by modulating oxidative stress and inflammatory responses, we evaluated how fructose feeding might affect the smoking-induced emphysema in mice. We found that chronic fructose intake induced destruction and remodeling of lung parenchyma and impairment of respiratory mechanics, which are associated with distinctive cytokine profiles in bronchoalveolar lavage fluid, blood plasma and skeletal muscle. The combined effects of chronic fructose intake and cigarette smoking on destruction of lung parenchyma are more pronounced than the effects of either alone. Excessive intake of fructose might directly cause pulmonary emphysema in mice rather than just altering its natural history by facilitating the installation of a low-grade systemic inflammatory milieu.

Highlights

Chronic Obstructive Pulmonary Disease (COPD) is a syndrome that comprises several distinct and overlapping phenotypes
We showed that chronic fructose loading promotes destruction and remodeling of lung parenchyma and impaired respiratory mechanics
Such alterations in the structure and function of lung parenchyma are associated with distinctive cytokine profiles in Bronchoalveolar lavage fluid (BALF), blood plasma and skeletal muscle

Summary

Introduction

Chronic Obstructive Pulmonary Disease (COPD) is a syndrome that comprises several distinct and overlapping phenotypes. The first one considers the systemic manifestations and comorbidities as the result of a systemic “spill-over” of the inflammatory and reparatory events occurring in the lungs of patients with COPD, while in the second hypothesis the COPD is viewed as a systemic inflammatory disease that involves multiple organs with the pulmonary manifestations being one of its facets[5]. Both hypotheses predict that attenuation of persistent inflammation will decrease. The severity of COPD and its extra-pulmonary manifestations despite their significant divergence regarding the primary source of the inflammatory events

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