Abstract
trans Palmitoleic acid (t-16:1n-7, or 16:1 t9 in the δ nomenclature usually applied to trans fatty acids and used herein) arouses great scientific interest because it has been suggested to serve as a biomarker for lower risks of type 2 diabetes and coronary artery disease. Although 16:1 t9 has been assumed to derive from dietary sources, we examined the hypothesis that 16:1 t9 might also be endogenously produced from its metabolic precursor vaccenic acid (t-18:1n-7 or 18:1 t11). We reevaluated fatty acid data obtained from one human intervention study and one cellular model in both of which 18:1 t11 was supplemented. Both studies have already been published, but to our knowledge, 16:1 t9 has not yet been considered. This reanalysis of the datasets was reasonable because a new methodology for identifying 16:1 cis and trans isomers allowed us to address the subject presented in this article. Data showed that the systemic or intracellular increase in 16:1 t9 was strongly correlated with the increase in 18:1 t11 after the dietary intake or cellular uptake of 18:1 t11. The conversion rate in humans was, on average, 17%. Our findings suggest that endogenous 16:1 t9 is not, as has been assumed, exclusively diet derived but may also be produced by the partial β oxidation of dietary 18:1 t11.
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