Elaidic acid (EA) generates dysfunctional high-density lipoproteins and consumption of EA exacerbates hyperlipidemia and fatty liver change in zebrafish.

SCOPE

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.

CONCLUSION

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.