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738.21 |
1 PMCH, UTMB, Rt 1220, 301 Univ Blvd, Galveston, TX, 77555,
2 UTMB, Rt 1220, 301 Univ Blvd, Galveston, TX, 77555
ABSTRACT
Background: Serious injury, including burn trauma, induces a hyper metabolic response and insulin resistance are still not well understood. Mitochondrial proteins and genes are damaged after burn injury in animals. However, mitochondrial function has not previously been assessed in human burn patients.
Methods: Muscle biopsies were taken from 40 children sustaining burns >40% of their body surface area and from 13 healthy children controls requiring non-emergent open abdominal surgery. The rates of maximal muscle mitochondrial oxidative capacity or ATP production and uncoupled oxidation or heat production for both palmitate and pyruvate were measured.
Results: Maximal mitochondrial oxidation of both pyruvate and palmitate were significantly reduced in burn patients compared to healthy controls (4.0¡Ó 0.2 vs. 1.9¡Ó0.1 
molO2/citrate synthase activity/mg protein/ min pyruvate; CON vs. BURN; P<0.001 and 3.0¡Ó 0.1 vs. 0.9¡Ó0.03 molO2/citrate synthase activity/mg protein/ min palmatyl CoA; CON vs. BURN; P=0.003 ). However, the rates of uncoupled oxidation were the same between the two groups. Thus the respiratory quotient index, or ratio of coupled to uncoupled oxidation was significantly higher in control subjects (4.9¡Ó0.2 vs. 1.9¡Ó0.1 pyruvate; P<0.001 CON vs. BURN and 3.9¡Ó0.2 vs. 1.4¡Ó0.1 palmitate; P<0.001 CON vs. BURN)
Conclusions: The maximal coupled mitochondrial oxidative capacity is severely impaired after burn injury, although there are no alterations in the rate of uncoupled oxidative capacity. It may be that the ratio of these indicates that a larger portion of energy production in trauma patients is wasted through uncoupling, rather than used for healing.
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