Pulmonary Function and Sleep Breathing: Two New Targets for Type 2 Diabetes Care

• Published in: Endocrine reviews Vol. 38; no. 6; pp. 550 - 573
• Main Authors: Lecube, Albert, Simó, Rafael, Pallayova, Maria, Punjabi, Naresh M, López-Cano, Carolina, Turino, Cecilia, Hernández, Cristina, Barbé, Ferran
• Format: Journal Article
• Language: English
• Published: Washington, DC Endocrine Society 01.12.2017; Oxford University Press
• Subjects: Abnormalities; Apnea; Autonomic nervous system; Breathing; Cystic fibrosis; Damage tolerance; Diabetes; Diabetes Complications - physiopathology; Diabetes mellitus; Diabetes mellitus (non-insulin dependent); Diabetes Mellitus, Type 2 - physiopathology; Diabetic neuropathy; Glucose; Glucose tolerance; Health risk assessment; Humans; Hypoxemia; Impact analysis; Inflammation; Insulin; Insulin resistance; Leptin; Lung - physiopathology; Lung diseases; Lungs; Metabolic pathways; Microvasculature; Neuropathy; Optimization; Patients; Population studies; Pulmonary functions; Respiration; Respiratory function; Respiratory Function Tests; Risk factors; Sleep; Sleep and wakefulness; Sleep Apnea Syndromes - physiopathology; Sleep disorders; Sleepiness
• ISSN: 0163-769X; 1945-7189
• DOI: 10.1210/er.2017-00173

Population-based studies showing the negative impact of type 2 diabetes (T2D) on lung function are overviewed. Among the well-recognized pathophysiological mechanisms, the metabolic pathways related to insulin resistance (IR), low-grade chronic inflammation, leptin resistance, microvascular damage, and autonomic neuropathy are emphasized. Histopathological changes are exposed, and findings reported from experimental models are clearly differentiated from those described in humans. The accelerated decline in pulmonary function that appears in patients with cystic fibrosis (CF) with related abnormalities of glucose tolerance and diabetes is considered as an example to further investigate the relationship between T2D and the lung. Furthermore, a possible causal link between antihyperglycemic therapies and pulmonary function is examined. T2D similarly affects breathing during sleep, becoming an independent risk factor for higher rates of sleep apnea, leading to nocturnal hypoxemia and daytime sleepiness. Therefore, the impact of T2D on sleep breathing and its influence on sleep architecture is analyzed. Finally, the effect of improving some pathophysiological mechanisms, primarily IR and inflammation, as well as the optimization of blood glucose control on sleep breathing is evaluated. In summary, the lung should be considered by those providing care for people with diabetes and raise the central issue of whether the normalization of glucose levels can improve pulmonary function and ameliorate sleep-disordered breathing. Therefore, patients with T2D should be considered a vulnerable group for pulmonary dysfunction. However, further research aimed at elucidating how to screen for the lung impairment in the population with diabetes in a cost-effective manner is needed.Current evidence supporting the link among type 2 diabetes, pulmonary dysfunction, and sleep disorders is reviewed. We conclude the lung is a new target for the deleterious effects of diabetes.