title: Burn Induces Browning of the Subcutaneous White Adipose Tissue in Mice and Humans.
abstract: Burn is accompanied by long-lasting immuno-metabolic alterations referred to as hypermetabolism that are characterized by a considerable increase in resting energy expenditure and substantial whole-body catabolism. In burned patients, the length and magnitude of the hypermetabolic state is the highest of all patients and associated with profoundly increased morbidity and mortality. Unfortunately, the mechanisms involved in hypermetabolism are essentially unknown. We hypothesized that the adipose tissue plays a central role for the induction and persistence of hypermetabolism post-burn injury. Here, we show that burn induces a switch in the phenotype of the subcutaneous fat from white to beige, with associated characteristics such as increased mitochondrial mass and UCP1 expression. Our results further demonstrate the significant role of catecholamines and interleukin-6 in this process. We conclude that subcutaneous fat remodeling and browning represent an underlying mechanism that explains the elevated energy expenditure in burn-induced hypermetabolism.
authors.affiliation: Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
authors.forename: David
authors.initials: D
authors.lastname: Patsouris
authors.affiliation: Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
authors.forename: Peter
authors.initials: P
authors.lastname: Qi
authors.affiliation: Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
authors.forename: Abdikarim
authors.initials: A
authors.lastname: Abdullahi
authors.affiliation: Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
authors.forename: Mile
authors.initials: M
authors.lastname: Stanojcic
authors.affiliation: Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
authors.forename: Peter
authors.initials: P
authors.lastname: Chen
authors.affiliation: Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Parousis
authors.affiliation: Sunnybrook Research Institute, Toronto, ON M4N 3M5, Canada; Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
authors.forename: Saeid
authors.initials: S
authors.lastname: Amini-Nik
authors.affiliation: Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Sunnybrook Research Institute, Toronto, ON M4N 3M5, Canada; Sunnybrook Research Institute, Toronto, ON M4N 3M5, Canada; Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada. Electronic address: marc.jeschke@sunnybrook.ca.
authors.forename: Marc G
authors.initials: MG
authors.lastname: Jeschke
mesh_terms: D052436:Adipose Tissue, White / Q000378:metabolism*; D000818:Animals; D002056:Burns / Q000378:metabolism*; D002395:Catecholamines / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D007473:Ion Channels / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008875:Middle Aged; D008928:Mitochondria / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000378:metabolism; D000071256:Uncoupling Protein 1
chemical_list: D002395:Catecholamines; D015850:Interleukin-6; D007473:Ion Channels; D024101:Mitochondrial Proteins; C000604371:UCP1 protein, human; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1