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

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Abstract

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.

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