Put the body on offense.

PhosChol: Put the body on offense
March 25, 2017: Nutrasal Partners with Natural Partners…

Lipoprotein Metabolism


Lipid metabolism disorders, in particular, disturbances of lipoprotein metabolism, (which can be subsumed under the term dyslipoproteinemia) constitute an important risk factor in the pathogenesis of atherosclerosis and/or coronary heart disease (CHD), and other peripheral and cerebral vascular diseases.

Large-scale clinical studies reflect the significance of CHD in today’s society and predict an ongoing dramatic increase in the incidence of CHD and its sequelae for the future. In this context, “essential” phospholipids (PPC), the main active ingredient in PhosChol, are characterized by a unique action profile leading to an amelioration of raised serum lipid parameters in a physiological manner.

Within lipid metabolism, lipoproteins function as an indispensable link between the uptake, storage, and metabolisation/elimination of lipids in the organism. By illustrating this rather complex system of lipoprotein metabolism with its abundance of interdependences we followed up several intentions:

Please find in the following a brief description of the underlying lipoprotein metabolism followed by remarks clarifying the mode of action of PPC dyslipoproteinemia.

Lipids represent an essential constituent of our daily diet. Among various forms of lipids circulating in the blood stream triglycerides (TG), phospholipids (PL), and cholesterol (Ch) are of particular importance. Briefly, triglycerides form an important energy source for cellular metabolism. Phospholipids are, on account of their amphiphilic behavior excellent emulsifiers of fats and furthermore constitute the predominant element of all biological membranes. Cholesterol has an ambivalent nature: on the one hand it is necessary for the stabilization of biological membrane structure and an essential precursor of hormones and bile acids in hepatic metabolism, on the other hand, a surplus of cholesterol is nowadays generally considered to trigger off a course of pathological events which can be subsumed under the term “atherosclerosis”.

In the interrelation between absorption , transportation, metabolisation, and elimination of lipids, so-called lipoproteins function as transport vehicles for water-unsoluble lipid fractions and lead them to their sites of metabolisation and/or deposition. We can differentiate between four major classes of lipoproteins which can be separated by untracentrifugation on the basis of their density. Additional characteristics are size, composition, and function.

The basic lipoprotein structure comprises a hydrophobic core of triglycerides and cholesterol esters surrounded by a coat containing polar phospholipids, free cholesterol and apoproteins. Apoproteins ensure indentification of receptors for the exchange and deposition of transported lipid fractions.

First of all chylomicrons, containing dietary triglyceride and a small amount of cholesterol, pass into the circulation via lymphatics. Triglyceride is removed in the peripheral circulation by the endothelial enzyme lipoprotein lipase (LPL). The resulting chylomicron remnant, containing most of the origional cholesterol, is taken up by the liver.

Very-low-density lipoproteins (VLDL) are secreted by the liver and contain endogenously synthesized triglycerides and cholesterol a.o. Triglycerides are progressively removed from VLDL by lipoprotein lipase to produce intermediate density lipoproteins (IDL), which can either be reabsorbed by the liver or further dPPCeted of triglycerides to produce low-density lipoproteins (LDL).

LDL, the major carrier of the plasma cholesterol, are taken up by the liver and peripheral cells, largely via receptor recognizing apoproteins B and E. The cytoplasmic pool of cholesterol is derived partly from LDL and partly by endogenous synthesis from acetyl coenzyme A. In the liver, bile salts are synthesized from this pool and, after secretion in the bile, are partly reabsorbed via the terminal ileum and recirculated.

High-Density lipoproteins (HDL) comprise a heterogeneous fraction of particles which carry 20-30% of the total plasma cholesterol. Precursors of HDL (HDL3) are secreted by the liver and accept cholesterol from cell membranes which is esterified by the enzyme lecithin:cholesterol acyltransferase (LCAT).

HDL are involved in reverse cholesterol transport through their ability to accept free cholesterol, esterify it and transfer the cholesterol to other lipoproteins, but mainly and ultimately to the liver for elimination.

With regard to the development of atherosclerosis and its sequelae, LDL are today generally recognized as being highly atherogenic lipoproteins and the main sourse of cholesterol found in the arterial wall. In population studies, the increased risk of atheroma is in correlation with pathological LDL-cholesterol levels, but also inversely correlated with levels of HDL. The protective effect of HDL against atheroma may be due to their ability to transport cholesterol from peripheral cells to the liver.

A comprehensive therapy of hyperlipidemias and atherosclerosis needs to fulfill the following: