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Central GLP-1 Resistance Induced by Severe Traumatic Brain Injury Was Associated with Persistent Hyperglycemia in
1Neurocritical Care Unit, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, China.
Insights
Higher plasma glucagon-like peptide-1 (GLP-1) levels in traumatic brain injury (TBI) patients predict mortality. This suggests central resistance to GLP-1 may contribute to hyperglycemia and poor outcomes in TBI survivors.
Area of Science:
- Neuroscience
- Endocrinology
- Critical Care Medicine
Background:
- The role of the glucagon-like peptide-1 (GLP-1) system in glucose homeostasis following traumatic brain injury (TBI) is not well understood.
- Investigating GLP-1's potential as a prognostic marker in TBI patients is crucial for understanding outcomes.
Purpose of the Study:
- To determine if plasma GLP-1 levels can differentiate between survivors and non-survivors within 14 days post-TBI.
- To assess the association of plasma GLP-1 levels with 6-month mortality in TBI patients.
Main Methods:
- Examined metabolic, inflammatory, and hematologic profiles in 73 TBI patients.
- Utilized two-way ANOVA to identify factors discriminating survivors from non-survivors.
- Employed binary logistic regression and Cox proportional hazard regression to determine biomarkers associated with mortality.
Main Results:
- Non-survivors exhibited higher 14-day plasma GLP-1, glucose, and IL-6 levels compared to survivors.
- Lower insulin levels at days 4-7 were observed in non-survivors.
- GLP-1 levels on days 8-10 and IL-6 on days 1-3 were positively associated with mortality, while insulin on days 4-7 was negatively associated.
Conclusions:
- Persistent elevated GLP-1 levels in non-survivors may indicate central resistance to GLP-1.
- This resistance could be linked to progressive hyperglycemia and increased mortality in TBI patients.
- Plasma GLP-1 levels show potential as a prognostic biomarker in TBI.
Introduction:
Whether central glucagon-like peptide 1 (GLP-1)/GLP-1 receptor system mediated peripheral glucose homeostasis in patients with traumatic brain injury (TBI) is not clear. We aim to determine if plasma GLP-1 level could distinguish the non-survivors from the survivors during the first 14 days after TBI that could prognose 6 months mortality.
Methods:
Metabolic, inflammatory, and hematologic profiles were examined in 73 patients with TBI in neurological intensive care unit. Factors that discriminate non-survivors from survivors were determined by two-way ANOVA. Biomarkers associated with mortality were determined by binary logistic regression and Cox proportional hazard regression.
Results:
The non-survivors had higher infectious SOFA scores (p < 0.001), lower first 3 days' body temperature (p = 0.017), greater chance of cerebral hernia (p = 0.048), and decompressive craniectomy (p = 0.001) than the survivors. Higher 14-day plasma GLP-1 (p < 0.0001), glucose (p = 0.002), and IL-6 (p = 0.005) levels, in contrast with lower insulin level at days 4-7 (p = 0.020) were found in non-survivors than in survivors. Except the survivors who had an increased 14-day platelet number (p < 0.001), the two groups did not differ in hematological profile and intestinal barrier function. Although GLP-1 correlated closely with IL-6 in both the groups, it correlated with neither insulin nor glucose in each group. GLP-1 on days 8-10 and IL-6 on days 1-3 were positively, while insulin on days 4-7 was negatively associated with mortality.
Conclusion:
Persistent higher GLP-1 level in non-survivors over the survivors may present more severe central resistance to endogenous GLP-1 in non-survivors, which may be associated with progressive hyperglycemia with increased mortality in TBI.
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