title: Effects of burn injury, cold stress and cutaneous wound injury on the morphology and energy metabolism of murine brown adipose tissue (BAT) in vivo.
abstract: OBJECTIVE
  Cold stress has been shown to produce dramatic increases in 2-fluoro-2-deoxy-D-Glucose ((18)FDG) accumulation by brown adipose tissue (BAT) in rodents. However, neither the effects of other types of stress on (18)FDG accumulation nor the effects of stressors on the accumulation of tracers of other aspects of energy metabolism have been evaluated. In this report we studied the effects of cold stress, burn injury and cutaneous wounds on murine BAT at the macroscopic, microscopic and metabolic level.
  
  
  METHODS
  Glucose metabolism was studied with (18)FDG, fatty acid accumulation was evaluated with trans-9(RS)-(18)F-fluoro-3,4(RS,RS)-methyleneheptadecanoic acid (FCPHA) and tricarboxcylic acid cycle (TCA) activity was evaluated with (3)H acetate.
  
  
  RESULTS
  All three stressors produced dramatic changes in BAT at the macroscopic and microscopic level. Macroscopically, BAT from the stressed animals appeared to be a much darker brown in color. Microscopically BAT of stressed animals demonstrated significantly fewer lipid droplets and an overall decrease in lipid content. Accumulation of (18)FDG by BAT was significantly (p<0.01) increased by all 3 treatments (Cold: ~16 fold, burn ~7 Fold and cutaneous wound ~14 fold) whereas uptake of FDG by white fat was unchanged. This effect was also demonstrated non invasively by μPET imaging. Although less prominent than with (18)FDG, BAT uptake of FCPHA and acetate were also significantly increased by all three treatments. These findings suggest that in addition to cold stress, burn injury and cutaneous wounds produce BAT activation in mice.
  
  
  CONCLUSIONS
  This study demonstrates brown fat activated by several stressors leads to increased uptake of various substrates.
authors.affiliation: Department of Surgery, Boston, Massachusetts 02114, USA. carter.ea@gmail.com
authors.forename: Edward A
authors.initials: EA
authors.lastname: Carter
authors.forename: Ali A
authors.initials: AA
authors.lastname: Bonab
authors.forename: Victoria
authors.initials: V
authors.lastname: Hamrahi
authors.forename: Justin
authors.initials: J
authors.lastname: Pitman
authors.forename: Daniel
authors.initials: D
authors.lastname: Winter
authors.forename: Lacey J
authors.initials: LJ
authors.lastname: Macintosh
authors.forename: Erika M
authors.initials: EM
authors.lastname: Cyr
authors.forename: Kasie
authors.initials: K
authors.lastname: Paul
authors.forename: John
authors.initials: J
authors.lastname: Yerxa
authors.forename: Walter
authors.initials: W
authors.lastname: Jung
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 / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D002056:Burns / Q000378:metabolism / Q000473:pathology*; D003080:Cold Temperature; D058639:Cold-Shock Response / Q000502:physiology; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology*; D015870:Gene Expression; D005947:Glucose / Q000378:metabolism; D007035:Hypothermia / Q000503:physiopathology; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D012867:Skin / Q000293:injuries / Q000378:metabolism / Q000473:pathology*; D000071256:Uncoupling Protein 1; D014947:Wounds and Injuries / Q000378:metabolism / Q000473:pathology*
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; D000071256:Uncoupling Protein 1; D005947:Glucose