Retroconversion of dietary trans-vaccenic (trans-C18:1 n-7) acid to trans-palmitoleic acid (trans-C16:1 n-7): proof of concept and quantification in both cultured rat hepatocytes and pregnant rats.

Trans-palmitoleic acid (trans-C16:1 n-7 or trans-Δ9-C16:1, TPA) is believed to improve several metabolic parameters according to epidemiological data. TPA may mainly come from direct intakes: however, data are inconsistent due to its very low amount in foods. Instead, TPA might arise from dietary trans-vaccenic acid (trans-C18:1 n-7, TVA), which is more abundant in foods. TVA chain-shortening would be involved, but formal proof of concept is still lacking to our knowledge. Therefore, the present study aimed at providing in vitro and in vivo evidence of TVA retroconversion to TPA. First, fresh rat hepatocytes cultured with growing doses of TVA were able to synthesize growing amounts of TPA, according to a 10% conversion rate. In addition, TPA was found in secreted triacylglycerols (TAG). Inhibiting peroxisomal β-oxidation significantly reduced TPA synthesis, whereas no effect was observed when mitochondrial β-oxidation was blocked. Second, pregnant female rats fed a TVA-supplemented diet free of TPA did metabolize dietary TVA, leading to detectable amounts of TPA in the liver. Apart from the brain, TPA was also found in all analyzed tissues, including the mammary gland. Hepatic peroxisomal β-oxidation of dietary TVA, combined with exportation of TPA under VLDL-TAG, may explain amounts of TPA in other tissues. In conclusion, dietary TVA undergoes peroxisomal β-oxidation and yields TPA. Thus, not only TPA circulating levels in humans can be explained by dietary TPA itself, but dietary TVA is also of importance.