Imatinib treatment improves hyperglycaemic dysregulation in severe COVID-19: a secondary analysis of blood biomarkers in a randomised controlled trial.

Publication date: Feb 29, 2024

SARS-CoV-2 can induce insulin resistance, which is, among others, mediated by adipose tissue dysfunction and reduced angiotensin-converting enzyme 2 (ACE2) enzymatic activity. In SARS-CoV-2-infected mice, the tyrosine kinase inhibitor imatinib attenuates inflammation and improves insulin sensitivity. Here, we report the effects of imatinib on incident hyperglycaemia, circulating levels of glucoregulatory proteins, longitudinal insulin sensitivity and ACE-2 enzymatic activity in 385 hospitalized COVID-19 patients who participated in a randomized, double-blind, placebo-controlled clinical trial. Patients with severe hyperglycaemia had similar demographics compared to those without, but required longer hospital stays and exhibited higher invasive ventilation and mortality rates. The incidence of severe hyperglycaemia was significantly lower in patients treated with imatinib, while insulin production and central insulin sensitivity were unaffected. Imatinib increased plasma angiotensin-2 and adiponectin levels, and decreased c-Jun N-terminal protein kinase 1 (JNK1), JNK2 and interleukin-6 levels. These findings suggest that imatinib restores endocrine control of peripheral glucose uptake in COVID-19.

Concepts Keywords
Biomarkers COVID-19
Hyperglycaemia Insulin resistance
Insulin Proteomics
Mice Respiratory failure
Unaffected

Semantics

Type Source Name
drug DRUGBANK Imatinib
disease MESH COVID-19
disease IDO blood
disease MESH insulin resistance
pathway KEGG Insulin resistance
drug DRUGBANK Angiotensin II
disease MESH inflammation
disease VO report
disease IDO production
disease MESH Respiratory failure

Original Article

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