Fig. 6

Schematic representation of the molecular effects of CLA on skeletal muscle. Induction of Scd1, a ER-bound enzyme, is the key point in the molecular mechanism of action of CLA in muscle. It is suggested a coordinated regulation of the expression of the genes represented. Fasn would drive fatty acids to Scd1 for unsaturation, which is enhanced by CLA. Then, dgat2 and Sptlc1 and 2, would be coordinated for the fate of these fatty acids toward the synthesis of triglycerides or specific sphingolipids, maybe acting as secondary signalling molecules. These molecular events are associated with a protective of role of stress in ER, because the mediators of ER stress signalling pathways, including UPR (unfolded protein response) and apoptosis markers, are decreased or not altered. FA, fatty acid; MUFA, monounsaturated fatty acid; TAG: triacylglycerol