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

## TL;DR

This study examines how stress-induced high blood sugar affects glucose transport genes in the muscles of critically ill patients.

## Contribution

The study reveals that stress-induced hyperglycemia is linked to reduced IRS1 gene expression in skeletal muscle.

## Key findings

- No differences in gene expression were found between patients with and without diabetes.
- Hyperglycemia above 200 mg/dL was associated with downregulated IRS1 expression.
- A glycemic gap of ≥80 mg/dL also correlated with IRS1 downregulation.

## Abstract

To explore the association between diabetes and stress-induced hyperglycemia
with skeletal muscle expression of key genes related to glucose
transport.

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.

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.

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.