OBJECTIVE: The present study was done to clarify the mechanism by which conjugated linoleic acid (CLA) induces fatty liver in mice and to attenuate this symptom by adding other dietary fatty acids. METHODS: Mice were given CLA short (12 h) or long (4 wk) term or given CLA with linoleic acid (LA) or gamma-linolenic acid (GLA) in the long term (4 wk). Total lipids, triacylglycerol, and prostaglandin E(2) (PGE(2)) levels in the liver were determined. RESULTS: A single administration of CLA significantly increased PGE(2) levels in the liver 12 h after administration. However, long-term administration of CLA significantly decreased the liver PGE(2) level and induced fatty liver. GLA increased PGE(2) levels, and coadministration with GLA, but not with LA, prevented the CLA-induced fatty liver. CONCLUSIONS: These data suggest that CLA initially stimulates PGE(2) production followed by depletion of PGE(2) sources in the liver. The fatty liver associated with PGE(2) reduction by CLA ingestion can be attenuated by GLA in mice.
OBJECTIVE: The present study was done to clarify the mechanism by which conjugated linoleic acid (CLA) induces fatty liver in mice and to attenuate this symptom by adding other dietary fatty acids. METHODS:Mice were given CLA short (12 h) or long (4 wk) term or given CLA with linoleic acid (LA) or gamma-linolenic acid (GLA) in the long term (4 wk). Total lipids, triacylglycerol, and prostaglandin E(2) (PGE(2)) levels in the liver were determined. RESULTS: A single administration of CLA significantly increased PGE(2) levels in the liver 12 h after administration. However, long-term administration of CLA significantly decreased the liver PGE(2) level and induced fatty liver. GLA increased PGE(2) levels, and coadministration with GLA, but not with LA, prevented the CLA-induced fatty liver. CONCLUSIONS: These data suggest that CLA initially stimulates PGE(2) production followed by depletion of PGE(2) sources in the liver. The fatty liver associated with PGE(2) reduction by CLA ingestion can be attenuated by GLA in mice.