The interaction of prostaglandin E₁ with serum lipoproteins possible role in cholesterol homeostasis

Abstract

Prostaglandin (PG) E1 significantly stimulates the rate of cholesterol esterification in plasma. This effect could be attributed to an enhancement by PGE1 of the interlipoprotein transfer of phosphatidylcholine and cholesteryl esters, i.e., the substrate and product of lecithin-cholesterol acyltransferase (LCAT). The enhancement effect appears to be due to a rearrangement of the lipoprotein surface induced by specific interaction of PGE1 with some apolipoproteins, although the binding capacity of serum lipoproteins for PGE1 was found to be rather weak. To explain these findings, an hypothetical non-equilibrium model was put forward. The purpose of the present article is to summarize available data on the PGE1-lipoprotein interaction.

A novel source of dihomo‐γ‐linolenic acid: Possibilities and limitations of DGLA production in the high‐density cultures of the Δ5 desaturase‐mutant microalga Lobosphaera incisa

“…The omega‐6 LC‐PUFA dihomo‐γ‐linolenic acid (DGLA, 20:3 n ‐6) is the immediate precursor of arachidonic acid (AA, 20:4 n ‐6). In the n ‐6 LC‐PUFA biosynthesis pathway, these LC‐PUFA give rise to distinctive biologically active eicosanoids such as DGLA‐derived prostaglandin E1 (PGE 1 ), which is assumed to reduce inflammation, modulate vascular reactivity and to play role in cholesterol homeostasis . DGLA offers potential for the treatment of inflammatory disorders including atopic eczema, psoriasis, asthma, atherosclerosis and arthritis as well as in suppressing cancerogenesis .…”