Male weanling Wistar rats (n = 15), weighing 200-220 g, were allocated for
6 wk to diets containing 1% (by weight) of conjugated linoleic acid (CLA),
either as the 9c,11 t-isomer, the 10t, 12c-isomer, or as a mixture containi
ng 45% of each of these isomers. The five rats of the control group receive
d 1% of oleic acid,instead. Selected enzyme activities were determined indi
fferent tissues after cellular subfractionation. None of the CLA-diet induc
ed a hepatic peroxisome-proliferation response, as evidenced by a lack of c
hange in the activity of some characteristic enzymes [i.e., acyl-CoA oxidas
e, CYP4A1, but also carnitine palmitoyltransferase-1 (CPT-I)] or enzyme aff
ected by peroxisome-proliferators (glutathione S-transferase). In addition
to the liver,;the activity of the rate-limiting beta-oxidation enzyme in mi
tochondria, CPT-I, did not change either in skeletal muscle or in heart. Co
nversely, its activity increased more than 30% in:the control value in epid
idymal adipose tissue of the animals fed the CLA-diets containing the 10t,
12c-isomer. Conversely, the activity of phosphatidate phosphohydrolase, a r
ate-limiting enzyme in glycerolipid neosynthesis, remained unchanged in adi
pose tissue. Kinetic studies conducted on hepatic CPT-I and peroxisomal acy
l-CoA oxidase with CoA derivatives predicted a different channeling of CLA
isomers through the mitochondrial or the peroxisomal oxidation pathways. In
conclusion, the 10t, 12c-CLA isomer seems to be more efficiently utilized
by the cells than its 9c,11 t homolog, though the Wistar rat species appear
ed to be poorly responsive to CLA diets for the effects measured.