ArticleFrontiers in medicine2026
A latent metabolic dysfunction phenotype integrating insulin resistance and leptin is associated with disease severity in COPD.
Article in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Chronic obstructive pulmonary disease (COPD) is increasingly recognised as a systemic condition in which metabolic dysfunction may influence disease severity and exacerbation risk. The combined effects of insulin resistance and leptin dysregulation on COPD outcomes remain incompletely defined. This study evaluated their associations with exacerbation burden, airflow limitation and patient-reported outcomes, and assessed the discriminative performance of HOMA-IR and serum leptin for identifying advanced disease. Methods: A cross-sectional observational study was conducted at a tertiary care centre in southern Romania, including 96 patients with COPD and 24 healthy controls. Fasting insulin and serum leptin were measured, and insulin resistance was assessed using HOMA-IR. Spirometry and patient-reported outcomes (CAT, mMRC and SGRQ-C) were assessed in COPD patients. Metabolic markers were analysed individually and as a latent metabolic dysfunction phenotype using generalized structural equation modelling (GSEM). Results: Compared with controls, COPD patients had higher HOMA-IR (+206.9%), insulin (+112.2%) and leptin (+52.8%) levels. Both HOMA-IR and leptin were inversely correlated with spirometric indices, with stronger associations observed for HOMA-IR. Within the COPD cohort, neither individual metabolic markers nor a latent metabolic dysfunction phenotype integrating HOMA-IR, body mass index and leptin was associated with annual exacerbation rate (latent factor IRR = 1.089, 95% CI: 0.841-1.410, Conclusions: Metabolic dysfunction is substantially more pronounced in COPD than in individuals without airflow obstruction and correlates with the degree of airflow limitation, but does not independently predict exacerbation frequency within the COPD population. HOMA-IR outperformed leptin as a marker of disease severity, a finding that requires further validation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.