Insulin improves alveolar-capillary membrane gas conductance in type 2 diabetes

OBJECTIVE - In type 1 diabetes, lung diffusing capacity for carbon monoxide (DL _CO) may be impaired, and insulin has been shown to be beneficial in cases in which near-normal metabolic control is achieved. An influence of insulin, per se, on the alveolar-capillary membrane conductance is unexplored. We aimed at testing this possibility. RESEARCH DESIGN AND METHODS - We studied 19 life-long nonsmoking, asymptomatic patients with type 2 diabetes and normal cardiac function, whose GHb averaged 6.2 ± 0.3% with diet and hypoglycemic drugs. DL _CO and its subcomponents (alveolar capillary membrane conductance [D _M] and pulmonary capillary blood volume available for gas exchange [Vc]), vital capacity (VC), forced expiratory volume 1 s (FEV ₁), cardiac output (CO), ejection fraction (EF), pulmonary wedge pressure (WPP), and pulmonary arteriolar resistance (PAR) were determined before and within 60 min after infusion of 50 ml saline + 10 IU of regular insulin or after saline alone on 2 consecutive days (random block design). Glycemia was kept at baseline levels during experiments by dextrose infusion. RESULTS - Percent of normal predicted DL _CO averaged 84.2 ± 7.9% and in 14 patients was <100%. Insulin infusion, not saline alone, improved (P <0.01) DL _CO (12%) and D _M (14%) and raised DL _CO to 98% of the normal predicted value. There were no variations in VC, FEV ₁ CO, EF, WPP, or PAR, suggesting that the influences of the hormone on gas transfer were not mediated by changes in spirometry, volumes, and hemodynamics of the lung. CONCLUSIONS - Several cases of type 2 diabetes present with increased impedance to gas transfer across the alveolar-capillary membrane, and hypoglycemic drugs do not prevent this inconvenience. Insulin, independently of the metabolic effects, acutely improves gas exchange, possibly through a facilitation of the alveolar-capillary interface conductance.