Arachidonic acid prevents fatty liver induced by conjugated linoleic acid in mice

Abstract

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.

Trans-10, cis-12-conjugated linoleic acid alters hepatic gene expression in a polygenic obese line of mice displaying hepatic lipidosis

“…Putative translocation of fatty acids from adipose to liver tissues could have masked changes in the ratios of saturated to unsaturated fatty acids result ing from de novo hepatic synthesis. Although we did not measure circulting non-esterified fatty acid concentration or composition, Oikawa and coworkers [38] observed an attenuation of CLA-induced hepatic lipidosis via arachidonic acid and this effect was not associated with altered NEFA concentration.…”

Stimulation of fat accumulation in hepatocytes by PGE2-dependent repression of hepatic lipolysis, β-oxidation and VLDL-synthesis

“…Efficient storage of fatty acids in triglycerides may actually protect the liver from adverse effects caused by high concentrations of circulating non-esterified fatty acids. 46,47 This could explain why in some in vivo experiments PGE 2 had beneficial effects on the development of NASH, 48,49 whereas others 32-34 (see above) rather support the view that PGE 2 has a negative impact on the development of steatosis.…”

Trans-10,cis-12-CLA-Caused Lipodystrophy Is Associated with Profound Changes of Fatty Acid Profiles of Liver, White Adipose Tissue and Erythrocytes in Mice: Possible Link to Tissue-Specific Alterations of Fatty Acid Desaturation

“…More likely, an active sup- pression of desaturation occurred, since t 10, c 12-CLA has been shown to reduce the ⌬ 6 and ⌬ 5 desaturation ratios in HepG2 cells [55,56] . Due to the fact that only marginal amounts of C20: 4(n-6) were detectable in the liver lipids of the CLA-mix diet group, the observation that coadministration of arachidonic acid to a CLA-mix diet averts the development of fatty livers in mice [57] is of outstanding interest. However, the underlying mechanism remains elusive.…”