Dados do Trabalho

Título

Association between diabetes and stress-induced hyperglycemia with skeletal muscle gene expression of IRS1, IRS2, INSR, SLC2A1, and SLC2A4 in critically ill patients

Objetivo

Stress-induced hyperglycemia is associated with the development of intensive care unit-acquired weakness (ICU-AW). This study aimed to investigate the association between diabetes and stress-induced hyperglycemia with skeletal muscle gene expression of IRS1, IRS2, INSR, SLC2A1, and SLC2A4 in critically ill patients.

Métodos

In this prospective cohort study, adult critically ill patients were included. Muscle biopsies were conducted and the expression levels of insulin receptor substrate 1 (IRS1), insulin receptor substrate 2 (IRS2), insulin receptor (INSR), solute carrier family 2 member 1 (SLC2A1), and solute carrier family 2 member 4 (SLC2A4), were analyzed using RT-qPCR. The study compared the gene expression between patients with and without DM. Secondary planned analyses were the comparison of gene expression of patients with or without stress-induced hyperglycemia.

Resultados

From April 2018 to September 2018, 50 patients were included. No significant differences in skeletal muscle gene expressions were found between patients with or without DM. Patients with glycemic variability ≥40 mg/dL exhibited a downregulation of INSR compared to <40 mg/dL (1.3 [0.01 – 5] vs. 2.1 [0.7 - 3.4] fold-changes, p=0.045). The same pattern was observed when glycemic gap threshold of 80 mg/dL was used (1.4 [0.25 – 5] vs 1 [0.01 - 2.3] fold-changes in patients with glycemic gap <80 mg/dL and ≥80 mg/dL respectively, p=0.015).

Conclusão

No significant changes in skeletal muscle gene expression of IRS1, IRS2, INSR, SLC2A1, and SLC2A4 were found in patients with or without diabetes. However, INSR was downregulated in the skeletal muscle of critically ill patients with stress-induced hyperglycemia.