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Table 2 Palmitate kinetics and Protein Kinase-C activation

From: PPAR-α agonism improves whole body and muscle mitochondrial fat oxidation, but does not alter intracellular fat concentrations in burn trauma children in a randomized controlled trial

  PLA FEN
Measurement Pre Post Pre Post
Palmitate oxidation     
   Basal 0.85 ± 0.19 1.03 ± 0.12 0.99 ± 0.13 1.40 ± 0.13*
   Clamp 0.32 ± 0.05† 0.44 ± 0.04†* 0.35 ± 0.05† 0.74 ± 0.13†*
Percent uptake oxidized     
   Basal 28 ± 3 28 ± 3 24 ± 2 30 ± 2*
   Clamp 27 ± 3 28 ± 1 27 ± 3 37 ± 5
Palmitate Release     
   Basal 2.96 ± 0.5 3.66 ± 0.3 4.06 ± 0.4 4.7 ± 0.3
   Clamp 1.20 ± 0.2† 1.94 ± 0.2† 1.15 ± 0.2† 2.04 ± 0.3†
PKC-β     
   Basal 0.35 ± 0.10 0.30 ± 0.11 0.25 ± 0.04 0.70 ± 0.25
   Clamp 1.12 ± 0.60 1.64 ± 0.70 1.99 ± 0.58 1.64 ± 0.46
PKC-θ     
   Basal 1.38 ± 0.27 1.15 ± 0.36 0.87 ± 0.28 1.26 ± 0.38
   Clamp 0.98 ± 0.17 1.15 ± 0.48 0.87 ± 0.31 0.33 ± 0.11*
  1. The rate of palmitate oxidation is shown in (μmol/kg/min), percent uptake oxidation and whole body palmitate release (μmol/kg/min). * indicates a change from pre to post treatment, and † represents a change from basal to clamp. Of interest was a significant increases in the rate of palmitate oxidation in the basal (P = 0.004) and clamp (P = 0.03) states following fenofibrate treatment, and the percent uptake oxidized (P = 0.04) Protein Kinase-C β membrane translocation is shown in relative units, representing activation in both the basal and the clamp hyper-insulinemic state following fenofibrate treatment. Protein Kinase-C θ membrane translocation, representing activation representing activation in both the basal and the clamp hyper-insulinemic state following fenofibrate treatment. * The activation of PKC-θ decreased significantly during hyper-insulinemia following fenofibrate treatment (P = 0.004).