Porter 2013 Abstract IOC75

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Porter C (2013) Severe thermal trauma alters adipose tissue mitochondrial function in children. Mitochondr Physiol Network 18.03.

Link: IOC75 Open Access

Porter C, Herndon DN, Radhakrishnan RS, Borsheim E, Sidossis LS (2013)

Event: IOC75

Severe thermal trauma results in a hypermetabolic stress response. Whether altered mitochondrial function plays a role in this response remains unknown. Here, coupled and uncoupled mitochondrial O2 consumption rates were determined in subcutaneous adipose tissue (AT) samples obtained from healthy children and children with severe burns.
Maximal coupled mitochondrial VO2 (Oxphos) was determined in Digitonin permeabilized subcutaneous AT samples from healthy children (7.8±2.3 years old, n=5), and children with severe burns (12.1±2.4 years old, 42±28 days post-burn, 55±17% total body surface area burned (n=19) (mean±SD), in the presence of excess substrates (octanoyl-carnitine, pyruvate, malate, glutamate, and succinate) and ADP. Maximal uncoupled mitochondrial VO2 (State 4 respiration) was subsequently determined following the addition of oligomycin.
Oxphos was 2-fold greater in AT samples from children with severe burns relative to healthy children (1.74±0.23 vs. 0.79±0.23 pmol/(mg*sec), P<0.05). In addition, state 4 respiration was 4-fold greater in severely burned children relative to healthy children (1.58±0.25 vs. 0.42±0.15 pmol/(mg*sec), P<0.05) (mean±SEM). Citrate synthase activity, a proxy of mitochondrial content, was 3-fold higher in burn patients (14.2±2.3 vs. 4.2±1.1 nmol/g/sec), P<0.05). The ratio of uncoupled to coupled respiration, independent of mitochondrial content, was significantly higher in burn patients (0.85±0.08 vs. 0.51±0.08, P<0.05).
These data are the first to show that severe burn injury alters subcutaneous AT mitochondrial function; where AT from burn patients have significantly greater Oxphos, which is explained by greater mitochondrial content. In addition, mitochondria have a greater capacity for uncoupled respiration in patients with severe burns, suggesting that severe burn injury results in quantitative and qualitative adaptations in AT mitochondria. These data suggest that altered AT mitochondrial function may play a role in the hypermetabolic stress response to burn injury.


O2k-Network Lab: US TX Galveston Porter C, US AR Little Rock Borsheim E


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Affiliations and author contributions

Supported by the National Institutes of Health (P50-GM60338 and RO1-GM056687) and Shriners Hospitals for Children grants (84090, 84085, 71006 71008 and 79135) grants. CP is partly supported by an Interdisciplinary Rehabilitation Research Postdoctoral Training Grant (H133P110012) from the National Institute of Disability and Rehabilitation Research and Department of Education.

Craig Porter1,2, David N Herndon1,2, Ravi S Radhakrishnan2 Elisabet BØrsheim1,2, and Labros S Sidossis1,3,4

  1. Metabolism Unit, Shriners Hospitals for Children – Galveston
  2. Department of Surgery, Shriners Hospitals for Children – Galveston
  3. Department Internal Medicine, Shriners Hospitals for Children – Galveston
  4. Institute of Translational Sciences, University of Texas Medical Branch at Galveston,Texas.


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