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Published on: February 7, 2018
Dietary supplementation with 11trans- and 12trans-18:1 and oxidative stress in humans
Katrin Kuhnt1, Andreas Wagner, Jana Kraft
1Institute of Nutrition, Friedrich Schiller University, Jena, Germany.
Background:
High consumption of trans fat has been associated with high oxidative stress in humans, which could increase the risk of the development or acceleration of several diseases, such as atherosclerosis, cancer, and type 2 diabetes.
Objective:
Several urinary and blood biomarkers of oxidative stress [8-iso-prostaglandin-F(2alpha) (PGF(2alpha)), 15-keto-dihydro-PGF(2alpha), and 7,8-dihydro-8-oxo-2'-deoxy-guanosine in urine and alpha-,beta-,gamma-,delta-tocopherol, and retinol in plasma] were monitored to evaluate the oxidative stress induced by dietary supplementation of 11trans- and 12trans-18:1 isomers in humans during a 6-wk intervention.
Design:
After a 14-d adaptation period free of trans fatty acid supplementation (baseline), the test group (n = 12) received 3.0 g 11trans-18:1/d and 3.0 g 12trans-18:1/d (Sigma 6.0 g/d), and the control group (n = 12) consumed a control oil free of trans fatty acids and conjugated linoleic acids for 6 wk.
Results:
The postintervention concentration of urinary 8-iso-PGF(2alpha) (free radical-induced lipid peroxidation) in the test group was significantly higher than baseline and significantly higher than that observed in the control group. The concentrations of 15-keto-dihydro-PGF(2alpha) (cyclooxygenase-mediated inflammatory response indicator) and 7,8-dihydro-8-oxo-2'-deoxy-guanosine (oxidative DNA damage) were not affected by the 11trans- and 12trans-18:1 supplementation.
Conclusions:
Although an increase in urinary 8-iso-PGF(2alpha) was observed and the effects of prolonged high (ie, >5.0 g/d) consumption of trans fat could be relevant to the development of disease, the mean intakes of 11trans- and 12trans-18:1 in Europeans are estimated to be significantly below the amounts administered in this study (ie, 6.0 g/d); such low intakes could minimize the possible risk of detrimental effects on human health.
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