McMaster University Medical Journal · Jul 26, 2026
Adipokine and biomarker profiles associated with post-burn white adipose tissue (WAT) browning and hypermetabolic response
By Chak C, Wojtowicz‐Piotrowski S, Jeschke MG
Background: Severe burn injury induces a sustained hypermetabolic state characterized by increased lipolysis, insulin resistance, muscle wasting, and white adipose tissue (WAT) browning. Although adipokines are central regulators of metabolic homeostasis, their association with post-burn WAT browning and hypermetabolism remains incompletely characterized. Objective: To examine the relationship between adipokine expression and markers of WAT browning and lipolysis following thermal injury using a murine model. Methods: A murine thermal injury model was used in 12-week-old mice. Inguinal WAT was harvested at 7 and 14 days post-burn alongside sham controls. RNA was isolated, reverse transcribed, and quantitative PCR was performed to assess expression of adipokines (AdipoQ, leptin, resistin, RBP4, NAMPT, ADISSP, CTHRC1, CPT1B) and markers of browning and lipolysis (UCP1, ATGL, HSL). Gene expression was analyzed relative to controls to evaluate temporal changes associated with hypermetabolism. Results: Burn injury induced a progressive increase in UCP1 expression (~3-fold at day 7; ~15-fold at day 14), confirming sustained WAT browning. ATGL expression increased at day 7, consistent with enhanced early lipolysis, but declined by day 14. AdipoQ, leptin, resistin, and RBP4 were consistently reduced at both timepoints, suggesting persistent adipokine dysregulation during the hypermetabolic response. NAMPT demonstrated a delayed reduction, significant at day 14. Preliminary analysis in aged mice revealed attenuated browning marker expression and distinct adipokine alterations compared to adults, suggesting age-dependent differences in metabolic adaptation. Conclusions: Thermal injury is associated with sustained WAT browning and concurrent suppression of key adipokines. These findings demonstrate a temporal association between adipokine dysregulation and post-burn metabolic remodeling, with potential age-related differences in adaptive capacity. Further studies evaluating circulating adipokines and mechanistic pathways may clarify their contribution to prolonged hypermetabolism and identify potential therapeutic targets.