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

• Published in: Clinical nutrition (Edinburgh, Scotland) Vol. 40; no. 2; pp. 632 - 637
• Main Authors: Zaher, Sara, Branco, Ricardo, Meyer, Rosan, White, Deborah, Ridout, Jenna, Pathan, Nazima
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.02.2021
• Subjects: Critical illness; Energy expenditure; GLP-1; Inflammation; Metabolism; Energy expenditure; Critical illness; Inflammation; GLP-1; Metabolism
• ISSN: 0261-5614; 1532-1983
• DOI: 10.1016/j.clnu.2020.06.013

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. 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. 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. 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.