Relationship between inflammation and metabolic regulation of energy expenditure by GLP-1 in critically ill children.

BACKGROUND & AIMS: Critical illness is associated with derangement in the metabolic and inflammatory response. Previous investigators have highlighted the cross-link between feeding, inflammation and gut homeostasis. Glucagon like peptide-1 (GLP-1) is a gut derived hormone that plays an important role in the modulation of energy metabolism through appetite regulation and promotion of gastric motility. Growing evidence suggests that GLP-1 might influence energy expenditure. The aim of this study was to assess the relationship between inflammatory activation and metabolic regulation of energy expenditure by assessing cytokine release, levels of GLP-1 and energy expenditure in a cohort of critically ill children.

METHOD

This is a prospective study conducted in critically ill children. A blood sample was collected from each child during the first few days of critical illness, for the analysis of serum inflammatory cytokines (TNF-α, IL-10, IL-6 and IL-1β) and GLP-1 in 42 children. Indirect calorimetry (IC) measurements were performed concurrently in a subset of 21 children. The metabolic index was determined using the ratio of Measured Resting Energy Expenditure (MREE)/Predicted Resting Energy Expenditure (PREE) based on the Schofield equation. Correlation analysis was performed, followed by a stepwise linear regression analysis to assess factors affecting GLP-1 and the metabolic index.

RESULTS

A total of 42 children (0-14 years) were included in this study. The regression analysis indicated that CRP, TNF-α, IL-6 and IL-1β statistically influenced GLP-1 concentrations (p < 0.01). Where IC measurements were performed (N = 21), GLP-1 showed a statistically significant association with the metabolic index (p < 0.01). No evidence of statistical association was recorded between the inflammatory mediators and the metabolic index. Overall the results showed that circulating GLP-1 was increased in response to inflammatory stimuli in critically ill children. GLP-1 contributed to the changes observed in MREE induced by critical illness in our cohort.

CONCLUSION

Energy expenditure is extremely variable in critically ill children, our study suggests that changes in GLP-1 might contribute to a significant amount of this variation. If confirmed in larger studies, GLP-1 could be used as a correction factor for REE predictive equations in critically ill children.