Anke Jaudszus1, Ronny Kramer, Maria Pfeuffer, Alexander Roth, Gerhard Jahreis, Katrin Kuhnt. 1. Department of Physiology and Biochemistry of Nutrition, Max Rubner-Institut, Federal Research Institute of Nutrition and Food, Karlsruhe, Germany (AJ, MP, and AR), and the Department of Nutritional Physiology, Institute of Nutrition, Friedrich Schiller University of Jena, Jena, Germany (RK, GJ, and KK).
Abstract
BACKGROUND: 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. OBJECTIVE: 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). DESIGN: 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. RESULTS: 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%. CONCLUSION: 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.
RCT Entities:
BACKGROUND: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. OBJECTIVE: 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). DESIGN: 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. RESULTS: 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%. CONCLUSION: 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.
Authors: Mohammad Y Yakoob; Peilin Shi; Frank B Hu; Hannia Campos; Kathryn M Rexrode; E John Orav; Walter C Willett; Dariush Mozaffarian Journal: Am J Clin Nutr Date: 2014-09-24 Impact factor: 7.045
Authors: Mohammad Y Yakoob; Peilin Shi; Walter C Willett; Kathryn M Rexrode; Hannia Campos; E John Orav; Frank B Hu; Dariush Mozaffarian Journal: Circulation Date: 2016-03-22 Impact factor: 29.690