Difference between revisions of "Porter 2015 Shock"
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{{Publication | {{Publication | ||
|title=Porter C, Herndon DN, Bhattarai N, Ogunbileje JO, Szczesny B, Szabo C, Toliver-Kinsky T, Sidossis LS (2015) Severe burn injury induces thermogenically functional mitochondria in murine white adipose tissue. Shock | |title=Porter C, Herndon DN, Bhattarai N, Ogunbileje JO, Szczesny B, Szabo C, Toliver-Kinsky T, Sidossis LS (2015) Severe burn injury induces thermogenically functional mitochondria in murine white adipose tissue. Shock 44:258-64. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/26009824 PMID: 26009824] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/26009824 PMID: 26009824] | ||
|authors=Porter C, Herndon DN, Bhattarai N, Ogunbileje JO, Szczesny B, Szabo C, Toliver-Kinsky T, Sidossis LS | |authors=Porter C, Herndon DN, Bhattarai N, Ogunbileje JO, Szczesny B, Szabo C, Toliver-Kinsky T, Sidossis LS | ||
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|journal=Shock | |journal=Shock | ||
|abstract=Chronic cold exposure induces functionally thermogenic mitochondria in the inguinal white adipose tissue (iWAT) of mice. Whether this response occurs in pathophysiological states remains unclear. The purpose of this study was to determine the impact of severe burn trauma on iWAT mitochondrial function in mice. Male balb-c mice (10-12 weeks) received full-thickness scald burns to ∼30% of the body surface area. iWAT was harvested from mice at 1, 4, 10, 20, and 40 days post injury. Total and uncoupling protein 1 (UCP1) dependent mitochondrial thermogenesis were determined in iWAT. Citrate synthase (CS) activity was determined as a proxy of mitochondria abundance. Immunohistochemistry was performed to assess iWAT morphology and UCP1 expression. UCP1 dependent respiration was significantly greater at 4 and 10 days post burn compared to sham, peaking at 20 days post burn (''P''<0.001). CS activity was 3-fold greater at 4, 10, 20 and 40 days post-burn versus sham (''P''<0.05). Per mitochondrion, UCP1 function increased after burn trauma (''P''<0.05). After burn trauma, iWAT exhibited numerous multilocular lipid droplets which stained positive for UCP1. The current findings demonstrate the induction of thermogenically competent mitochondria within rodent iWAT in a model of severe burn trauma. These data identify a specific pathology which induces the browning of WAT ''in vivo'', and may offer a mechanistic explanation for the chronic hypermetabolism observed in burn victims. | |abstract=Chronic cold exposure induces functionally thermogenic mitochondria in the inguinal white adipose tissue (iWAT) of mice. Whether this response occurs in pathophysiological states remains unclear. The purpose of this study was to determine the impact of severe burn trauma on iWAT mitochondrial function in mice. Male balb-c mice (10-12 weeks) received full-thickness scald burns to ∼30% of the body surface area. iWAT was harvested from mice at 1, 4, 10, 20, and 40 days post injury. Total and uncoupling protein 1 (UCP1) dependent mitochondrial thermogenesis were determined in iWAT. Citrate synthase (CS) activity was determined as a proxy of mitochondria abundance. Immunohistochemistry was performed to assess iWAT morphology and UCP1 expression. UCP1 dependent respiration was significantly greater at 4 and 10 days post burn compared to sham, peaking at 20 days post burn (''P''<0.001). CS activity was 3-fold greater at 4, 10, 20 and 40 days post-burn versus sham (''P''<0.05). Per mitochondrion, UCP1 function increased after burn trauma (''P''<0.05). After burn trauma, iWAT exhibited numerous multilocular lipid droplets which stained positive for UCP1. The current findings demonstrate the induction of thermogenically competent mitochondria within rodent iWAT in a model of severe burn trauma. These data identify a specific pathology which induces the browning of WAT ''in vivo'', and may offer a mechanistic explanation for the chronic hypermetabolism observed in burn victims. | ||
|mipnetlab=US TX Galveston Porter C, US TX Galveston Sheffield-Moore M | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
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|organism=Mouse | |organism=Mouse | ||
|tissues=Fat | |tissues=Fat | ||
|preparations=Permeabilized tissue | |||
|couplingstates=LEAK | |||
|pathways=F, N, S, NS, Other combinations | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Latest revision as of 09:51, 8 November 2016
| Porter C, Herndon DN, Bhattarai N, Ogunbileje JO, Szczesny B, Szabo C, Toliver-Kinsky T, Sidossis LS (2015) Severe burn injury induces thermogenically functional mitochondria in murine white adipose tissue. Shock 44:258-64. |
Porter C, Herndon DN, Bhattarai N, Ogunbileje JO, Szczesny B, Szabo C, Toliver-Kinsky T, Sidossis LS (2015) Shock
Abstract: Chronic cold exposure induces functionally thermogenic mitochondria in the inguinal white adipose tissue (iWAT) of mice. Whether this response occurs in pathophysiological states remains unclear. The purpose of this study was to determine the impact of severe burn trauma on iWAT mitochondrial function in mice. Male balb-c mice (10-12 weeks) received full-thickness scald burns to ∼30% of the body surface area. iWAT was harvested from mice at 1, 4, 10, 20, and 40 days post injury. Total and uncoupling protein 1 (UCP1) dependent mitochondrial thermogenesis were determined in iWAT. Citrate synthase (CS) activity was determined as a proxy of mitochondria abundance. Immunohistochemistry was performed to assess iWAT morphology and UCP1 expression. UCP1 dependent respiration was significantly greater at 4 and 10 days post burn compared to sham, peaking at 20 days post burn (P<0.001). CS activity was 3-fold greater at 4, 10, 20 and 40 days post-burn versus sham (P<0.05). Per mitochondrion, UCP1 function increased after burn trauma (P<0.05). After burn trauma, iWAT exhibited numerous multilocular lipid droplets which stained positive for UCP1. The current findings demonstrate the induction of thermogenically competent mitochondria within rodent iWAT in a model of severe burn trauma. These data identify a specific pathology which induces the browning of WAT in vivo, and may offer a mechanistic explanation for the chronic hypermetabolism observed in burn victims.
• O2k-Network Lab: US TX Galveston Porter C, US TX Galveston Sheffield-Moore M
Labels: MiParea: Respiration
Organism: Mouse
Tissue;cell: Fat
Preparation: Permeabilized tissue
Coupling state: LEAK
Pathway: F, N, S, NS, Other combinations
HRR: Oxygraph-2k
