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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).