Submitted on March 24, 2006
Revised on June 13, 2006
Accepted on June 30, 2006
Conjugated linoleic acid (CLA) and hepatic lipogenesis in mouse: Role of the mitochondrial citrate carrier
Alessandra Ferramosca, Viviana Savy, Laura Conte, Sara Colombo, Alexandra W.C. Einerhand, and Vincenzo Zara
DISTEBA, University of Lecce, Lecce 73100
Corresponding Author: vincenzo.zara{at}unile.it
Conjugated linoleic acid or CLA is able to reduce adiposity by affecting lipid metabolism. In particular, CLA administration to mice reduces body fat mass with a concomitant lipid accumulation in the liver. We investigated the effects of CLA on the activity of the mitochondrial citrate carrier (CIC) which is implied in hepatic lipogenesis. The transport activity of the CIC, measured both in intact mitochondria and in the proteoliposomes, progressively increased with the duration of the CLA-feeding. An increase in the CIC activity of about 1.7 fold was found in the 16 weeks CLA-treated mice with respect to control animals. A kinetic analysis showed a 1.6 fold increase in the Vmax of citrate transport, but no change in the Km value. Western blot experiments revealed an increase of about 1.7 fold in the expression of CIC following CLA treatment. A strict correlation between the increase in the CIC activity and the stimulation of the cytosolic lipogenic enzymes was also found. These data indicate that the mitochondrial CIC may play a role in the onset of the hepatic steatosis in CLA-fed mice by supplying the carbon source for the de novo fatty acid synthesis.
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