Inhibition of hydrolysis of palmitic and oleic triglycedires (TG) in
very low density lipoproteins (VLDL), slow formation of active apoВ-100 conformation, blockade of апоЕ/В-100
ligand formation in VLDL and their reduced uptake by
insulin-dependent cells cause
hypertriglyceridemia (HTG). Palmitic and oleic VLDL (>80% total VLDL) are not converted in
low density lipoproteins (
LDL).
Atherosclerosis is not an alimentary deficiency of polyenic
fatty acids (PFA), but results from low in vivo bioavailability of PFA in
LDL against the background of high dietary palmitic FA and palmitic
LDL. Plasma PFA content and cellular PFA deficiency are as high as
LDL cholesterol (CL). Primary prevention of
atherosclerosis should be based on a decrease in dietary content of palmitic saturated FA, trans FA and a moderate increase in PFA. It seems highly unlikely that the xeobiotics
statins,
fibrates and
probucol produce pleiotropic
biological effects in vivo. These effects are brought about by phylogenetically early humoral mediators
eicosanoids:
prostacyclins,
prostaglandins,
thromboxanes,
leukotrienes, and resolvins. It is reasonable to suggest that all preparations which act according to the same algorithm activate TG hydrolysis in VLDL and normalize cellular uptake of PFA in linoleic and linolenic
LDL via apoВ-100 endocytosis.
Atherosclerosis is a syndrome of cellular deficiency of essential polyenic FA.