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in heart mitochondria, while the PI was decreased by 31% in SKM and by 17% in
heart mitochondria.
Figure 1.-‐
Oleic (18:1n-‐9), Docosahexanoic (22:6n-‐3) and Peroxisomal Beta-‐Oxidation (22:6/24:6
ratio) from control and atenolol treated mice. Values are means ± SEM from 5-‐6 (heart) or 6 (SKM)
different animals and are expressed as percentage of those in the controls for each parameter.
Control values: 12.85±0.76 (18:1n-‐9, heart); 28.03±1.01 (22:6n-‐3, heart); 187.94±19.46 (22:6/24.6,
heart); 16.39±0.47 (18:1n-‐9, SKM); 21.29±0.53 (22:6n-‐3, SKM); 103.44±10.32 (22:6/24.6, SKM).
Asterisks represent significant differences between the control and the atenolol group. * P<0.05; **
P<0.01; *** P<0.001.
Figure 2.-‐
Metabolic pathway from fatty acids of the n-‐3 serie. The name of the mouse enzymes
likely to contribute to elongation (ELOVL 2 and 5) and desaturation (Stearoyl-‐CoA desaturase,
SCDs) steps are indicated in these pathway.
