Amarin Corp Plc (AMRN)

[Pyrrhonian]

First off DHA has little effect on negating oxLDL-C, sorry buddy! But back to the drawing board for you! --BioC

Actually:

Enhanced uptake of free fatty acids (FFA) and oxidised low-density lipoproteins (oxLDL) may lead to oxidative stress and microvascular dysfunction interacting with CD36, a PPARa/?-regulated scavenger receptor and long-chain FFA transporter. We investigated CD36 expression and CD36-mediated oxLDL uptake before and after insulin treatment in human dermal microvascular endothelial cells (HMVECs), ± different types of fatty acids (FA), including palmitic, oleic, linoleic, arachidonic, eicosapentaenoic (EPA), and docosahexaenoic (DHA) acids.

A ≥ 24 hour exposure to 50 µM DHA or EPA, but not other FA, blunted both the constitutive (by 23 ± 3% and 29 ± 2%, respectively, p<0.05 for both) and insulin-induced CD36 expressions (by 45 ± 27 % and 12 ± 3 %, respectively, p<0.05 for both), along with insulin-induced uptake of DiI-oxLDL and the downregulation of phosphorylated endothelial nitric oxide synthase (P-eNOS).

At gel shift assays, DHA reverted insulin-induced basal and oxLDL-stimulated transactivation of PPRE and DNA binding of PPARa/? and NF-?B.

Etc. Still warring against DHA because you think that benefits your AMRN long thesis I see :)

Please review:

DHA has proven beneficial in a variety of ways that are significant to cardiac care, including:

-raises HDL-C (EPA probably does not, and very high doses of EPA without DHA may have an adverse effect on HDL-C)
-impedes oxLDL uptake to a greater degree than EPA
-helps lower TG and VLDL better than EPA alone (EPA 4g vs EPA 2g+DHA 2g)
-positively affects elevated blood pressure and heart rate (EPA does not)
-DHA (but not EPA) is a potent suppressor of SREBP-1, which is intimately tied to processes of atherosclerosis
-DHA increases the size of LDL particles, making them less atherogenic

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GL