Stress-induced hyperglycemia and expression of glucose cell transport genes in skeletal muscle of critically ill patients: a cross-sectional study

应激诱导的高血糖症及危重患者骨骼肌中葡萄糖细胞转运基因的表达:一项横断面研究

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Abstract

OBJECTIVE: To explore the association between diabetes and stress-induced hyperglycemia with skeletal muscle expression of key genes related to glucose transport. METHODS: This is a cross-sectional study. Skeletal muscle biopsies were taken from the left vastus muscle of critically ill adult patients within 24 hours of intensive care unit admission, and the expression of the genes of interest, namely insulin receptor substrate 1 (IRS1), insulin receptor substrate 2 (IRS2), solute carrier family 2 member 1 (SLC2A1), and solute carrier family 2 member 4 (SLC2A4), was analyzed using quantitative polymerase chain reaction. The primary analysis was planned to compare the gene expression pattern between patients with and without diabetes mellitus. The secondary analyses compared the gene expression in subgroups of patients with different levels of glycemia, glycemic variability, and glycemic gap. RESULTS: A total of 50 consecutive patients (15 with diabetes mellitus and 35 without diabetes mellitus) were included from April 2018 to September 2018. No differences in gene expression were found between patients with or without diabetes mellitus. Individuals with hyperglycemia > 200 mg/dL at intensive care unit admission exhibited a downregulation of IRS1 compared to those without (0.4 [0.1-0.8] versus 1.1 [0.3-2.2], p = 0.04). Similarly, patients with a glycemic gap ≥ 80 mg/dL exhibited a downregulation of IRS1 compared to those with a glycemic gap < 80 mg/dL (0.3 [0.1-0.7] versus 1 [0.4-2] p=0.04). There was no difference in gene expression between patients with glycemic variability higher or lower than 40 mg/dL. CONCLUSION: No significant changes were found in skeletal muscle expression of IRS1, IRS2, SLC2A1, and SLC2A4 in critically ill patients with or without diabetes mellitus. However, IRS1 was downregulated in patients with stress-induced hyperglycemia.

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