Conjugated linoleic acid (CLA) has anti-obesity effects, but induces fatty liver in mice. The present study investigated whether co-administration of arachidonic acid (ARA) attenuates fat accumulation in the mouse liver induced by CLA. Male mice (8 weeks old) were given diets with either no addition of dietary fat (control), 3 % linoleic acid (LA), 3 % CLA, 3 % CLA þ 1 % ARA, or 3 % CLA þ 2 % ARA for 4 weeks. The perirenal fat weight in ARA-treated groups decreased similarly as with CLA alone, when compared to control or LA. Plasma TAG concentration was significantly higher in the CLA group than in either CLA þ ARA group, while plasma cholesterol and NEFA concentrations did not vary among the groups. In contrast to visceral fat, liver weight was significantly higher in the CLA group than in the control or LA groups, and the effects of CLA were attenuated by ARA. TAG and cholesterol were markedly accumulated in the liver with dietary CLA, whereas co-administration with ARA, at either concentration, suppressed CLA-induced lipid accumulation. Liver PGE 2 was enhanced by a combination of CLA and ARA when compared with CLA alone, but PGE 1 level was not significantly different among groups. In conclusion, fatty liver induced by CLA was attenuated by co-administration with ARA, furthermore, a combination of these fatty acids maintained the anti-obese effect of CLA.

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Conjugated linoleic acid (CLA) has a role of biogenic regulation through modifying prostaglandin production. However, its effects on related metabolites of arachidonate remain unclear. Therefore, the effects of CLA on brain endocannabinoid content as well as its analogs were investigated. Mice (3-week-old), provided with diets containing 3% linoleic acid or 3% CLA for 4 weeks, were sacrificed and lipids were extracted from their cerebral cortex and hypothalamus. The amounts of N-arachidonoyl-ethanolamide, 2-arachidonoyl-glycerol (2-AG), oleoyl-ethanolamide and palmitoyl-ethanolamide were determined quantitatively by LC-MS. The 2-AG level in the cerebral cortex was significantly decreased by CLA treatment, but the other compounds were unaffected in the cerebral cortex and hypothalamus. The present study indicated that dietary CLA site-selectively decreases 2-AG in the cerebral cortex.

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The two principal endocannabinoids, N-arachidonoyl-ethanolamine (anandamide) and 2-arachidonoyl-glycerol (2-AG), are synthesized from arachidonic acid (AA) and AA is released as they are degraded. Therefore, the function of endocannabinoids is closely linked to AA, but the exact relationships have not been clarified, especially with respect to endocannabinoid metabolism. In the present study, oil rich in AA was administered (0, 100, 200 and 300 microl) orally to male mice for 7 days. Phospholipase D (PLD), fatty acid amide hydrolase (FAAH), diacyl-glycerol lipase (DAGL), monoacyl-glycerol lipase (MAGL) and cannabinoid 1 (CB1) receptor mRNA expressions were determined in the whole brain. No changes in the expression of any gene investigated were detected following AA treatment. However, it was demonstrated that the expression of the CB1 receptor was positively correlated with PLD, FAAH and DAGL expression. This suggests that expression of the CB1 receptor is closely coordinated with that of the enzymes which synthesize its ligands.