Porter 2015 Shock
|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.|
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.
Labels: MiParea: Respiration
Organism: Mouse Tissue;cell: Fat Preparation: Permeabilized tissue
Coupling state: LEAK Pathway: F, N, S, NS, Other combinations HRR: Oxygraph-2k