These authors have contributed equally to this work.
Elaidic acid (EA) generates dysfunctional high-density lipoproteins and consumption of EA exacerbates hyperlipidemia and fatty liver change in zebrafish
Article first published online: 26 MAY 2014
© 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Volume 58, Issue 7, pages 1537–1545, July 2014
How to Cite
Park, K.-H., Kim, J.-M. and Cho, K.-H. (2014), Elaidic acid (EA) generates dysfunctional high-density lipoproteins and consumption of EA exacerbates hyperlipidemia and fatty liver change in zebrafish. Mol. Nutr. Food Res., 58: 1537–1545. doi: 10.1002/mnfr.201300955
- Issue published online: 1 JUL 2014
- Article first published online: 26 MAY 2014
- Manuscript Accepted: 7 APR 2014
- Manuscript Revised: 16 MAR 2014
- Manuscript Received: 19 DEC 2013
- Mid-carreer Researcher Program. Grant Number: 2011-0015529
- Basic Science Research Program. Grant Number: 2010-020910
- National Research Foundation of Korea (NRF)
- Elaidic acid;
- Trans-fatty acid;
It is well known that trans-fatty acids have proatherogenic properties while HDL has antiatherogenic activities in plasma. However, there has been no report on the effects of trans-fat on the functional and structural properties of HDL.
Methods and results
To compare physiological properties, we synthesized reconstituted HDL (rHDL) containing stearic acid (18:0), oleic acid (18:1, cis), or elaidic acid (EA, 18:1, trans). An rHDL containing EA (EA-rHDL) showed loss of antioxidant ability and induced the highest uptake of oxidized LDL into human macrophages. EA-rHDL caused the strongest cellular senescence in human dermal fibroblast cells along with the highest production of inflammatory species in macrophages co-treated with fructose. Injection of EA-rHDL into zebrafish embryos resulted in acute embryonic toxicity with the lowest survivability. Consumption of trans-fat for 20 weeks resulted in remarkable hyperlipidemia, elevation of serum cholesteryl ester transfer protein activity, hepatic inflammation, and fatty liver changes.
Incorporation of EA impaired the beneficial effects of rHDL against atherogenesis. In zebrafish, EA-rHDL resulted in acute embryonic toxicity, and consumption of EA caused remarkable hyperlipidemia, inflammation, and fatty liver changes.