Introduction & Objective: Diabetes and SARS-CoV-2 infection target the endothelium causing perfusion abnormalities. We hypothesized that COVID-19 impairs insulin action and/or insulin secretion, and that systemic endothelial injury (EI) slows post-hospitalization recovery of these parameters.
Methods: 20 hospitalized adults with COVID-19 and acute hypoxemia (8 with DM) were tested for markers of endothelial function (hospital discharge, 1, 3 months) and oral glucose tolerance tests (OGTT) (1 and 3 months). Insulin sensitivity and insulin & C-peptide secretion metrics were assessed with empirical models (HOMA β, HOMA-IR) and mathematical ordinary differential equation (ODE) based models [(ISS (Sigma, SI), CSR (CSR0 (fasting), CSR-km (non-fasting)), ISR (ISR-km (non-fasting)), and ultradian ULS (a1, Rg)].
Results: Table 1 indicates significant correlations between patient-specific changes normalized over time (slopes) in EI and endocrine metrics. Uncertainty was estimated with linear mixed models adjusted for diabetes status and sex, respectively for each metric. Individually paired marker and metric slopes characterizing changes in participant physiological states were associated using linear regression models. Significance of predictive impact was interpreted from associated p-values of each slope pairing.
Conclusion: Changes in EI predict post-hospital recovery of carbohydrate metabolism.
J.E.B. Reusch: Advisory Panel; Medtronic. D. Albers: None. Y. Wang: None. J. Briggs: None. R. Maicki: None. J. Stroh: None. A. Gupta: None. A. Garcia: None. V. Singh: None. T.D. Hiller: None. A. Sherman: None. N. Rasouli: Advisory Panel; Eli Lilly and Company, Novo Nordisk. Research Support; Novo Nordisk. I.S. Douglas: None.
R01 DK130351
