Estimated glucose disposal rate exhibits an L-shaped threshold effect on small airway dysfunction in patients with type 2 diabetes

Background This study examined whether estimated glucose disposal rate (eGDR) is associated with small airway dysfunction (SAD) in type 2 diabetes (T2DM), aiming to inform early preventive strategies for pre-chronic obstructive pulmonary disease in this population. Methods Data from 567 patients with type 2 diabetes were analyzed in this retrospective cross-sectional study. The diagnostic criteria for SAD required a minimum of two out of three pulmonary function parameters, namely maximal mid-expiratory flow (MMEF), forced expiratory flow at 50% (FEF50%), and forced expiratory flow at 75% (FEF75%), to register values beneath the 65% threshold of their respective predicted norms. Multivariable logistic regression, restricted cubic splines (RCS) for nonlinear shape, piecewise logistic regression for threshold effect analysis, subgroup analysis with interaction tests were used to evaluate the relationship between eGDR and SAD. Results SAD was present in 91 patients (16.05%). Mean age was 55.23 ± 10.58 years, and mean diabetes duration was 10.73 ± 7.14 years. Multivariable logistic regression demonstrated that per 1-unit increment in eGDR as a continuous variable corresponded to 12% lower odds of SAD (OR=0.88, 95% CI: 0.79-0.98, p =0.025). Compared with the lowest quartile (Q1), the higher three quartiles (Q2–Q4) all showed significantly lower odds of SAD (all p < 0.05), with a significant dose-response trend ( p for trend=0.028). RCS analysis revealed a nonlinear inverse relationship approximating an “L-shaped” pattern ( p for nonlinearity=0.019). Exploratory threshold effect analysis demonstrated that below 5.67, every 1-unit rise in eGDR corresponded to 42% lower odds of SAD (OR = 0.58, 95%CI: 0.42-0.80, p < 0.001), whereas no significant association was observed above 5.67 ( p =0.413). Subgroup analyses by sex, smoking status, age (≥60 vs <60 years), diabetes duration (≥10 vs <10 years), BMI (≥24 vs <24 kg/m²), and diabetes-related complications consistently showed that higher eGDR was associated with lower odds of SAD, with no significant interaction (all p for interaction > 0.05). Conclusion In patients with T2DM, eGDR showed an “L-shaped” nonlinear inverse association with SAD. An exploratory threshold of 5.67 may identify patients with higher odds of SAD, with a plateau above this value. Further prospective studies and external validation are needed to explore its clinical value.