title: Brown adipose tissue and its modulation by a mitochondria-targeted peptide in rat burn injury-induced hypermetabolism.
abstract: Hypermetabolism is a prominent feature of burn injury, and altered mitochondria function is presumed to contribute to this state. Recently, brown adipose tissue (BAT) was found to be present not only in rodents but also in humans, and its activity is associated with resting metabolic rate. In this report, we elucidate the relationship between burn injury-induced hypermetabolism and BAT activity and the possible role of the mitochondria-targeted peptide SS31 in attenuating burn injury-induced hypermetabolism by using a rat burn injury model. We demonstrate that burn injury induces morphological changes in interscapular BAT (iBAT). Burn injury was associated with iBAT activation, and this effect was positively correlated with increased energy expenditure. BAT activation was associated with augmentation of mitochondria biogenesis, and UCP1 expression in the isolated iBAT mitochondria. In addition, the mitochondria-targeted peptide SS31 attenuated burn injury-induced hypermetabolism, which was accompanied by suppression of UCP1 expression in isolated mitochondria. Our results suggest that BAT plays an important role in burn injury-induced hypermetabolism through its morphological changes and expression of UCP1.
authors.affiliation: Shriners Hospitals for Children, Boston, 51 Blossom St., Boston, MA 02114, USA. aajjff@gmail.com
authors.forename: Kikuo
authors.initials: K
authors.lastname: Yo
authors.forename: Yong-Ming
authors.initials: YM
authors.lastname: Yu
authors.forename: Gaofeng
authors.initials: G
authors.lastname: Zhao
authors.forename: Ali A
authors.initials: AA
authors.lastname: Bonab
authors.forename: Naoki
authors.initials: N
authors.lastname: Aikawa
authors.forename: Ronald G
authors.initials: RG
authors.lastname: Tompkins
authors.forename: Alan J
authors.initials: AJ
authors.lastname: Fischman
mesh_terms: D002001:Adipose Tissue, Brown / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D000818:Animals; D002056:Burns / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D015536:Down-Regulation / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D007473:Ion Channels / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008297:Male; D046529:Microscopy, Electron, Transmission; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D028361:Mitochondrial Diseases / Q000209:etiology / Q000517:prevention & control*; D024101:Mitochondrial Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D063269:Mitochondrial Turnover / Q000187:drug effects; D058990:Molecular Targeted Therapy; D009842:Oligopeptides / Q000627:therapeutic use*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012540:Scapula; D013047:Specific Pathogen-Free Organisms; D000071256:Uncoupling Protein 1; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D016166:Free Radical Scavengers; D007473:Ion Channels; D024101:Mitochondrial Proteins; D009842:Oligopeptides; C000604371:UCP1 protein, human; C000604373:Ucp1 protein, rat; D000071256:Uncoupling Protein 1; C506540:arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide