Subfractional alterations of high density lipoproteins (HDL) were studied after incubation of blood serum from patients with normal lipid spectrum and with four types of dyslipidemia (hypercholesterolemia, hypertriglyceridemia, hypo- and hyper-alpha-cholesterolemia) in mixtures containing human skin fibroblasts and G-2 hepatoma cells used as typical populations of peripheric and liver cells. Incubation of normolipidemic blood sera with fibroblasts overloaded with cholesterol led to conversion of small HDL3 particles into large HDL2 subfractions arising due to the lipoprotein acception of cholesterol. At the same time, incubation of these blood sera with the hepatoma cells resulted in a decrease of the large particles ratio in total pool of HDL because of their absorption by the cells. No distinct differences were detected in formation of large particles from small subfractions when cholesterol was accepted from fibroblasts under conditions of hypercholesterolemia, hypertriglyceridemia and hyper-alpha-cholesterolemia, while formation of the largest particles HDL2b was impaired in hypo-alpha-cholesterolemia. These HDL2b particles interacted less effectively with hepatoma cells, thus suggesting the decreased cholesterol transport function of HDL in hypo-alpha-cholesterolemia. Content of HDL2b in total pool of HDL was unaltered if blood serum from patients with hyper-alpha-cholesterolemia was incubated together with the hepatoma cells. Antiatherogenic effect of hyper-alpha-cholesterolemia was caused mainly by active transfer of cholesterol from low density lipoproteins to HDL and a decrease in the LDL concentration but not by increased absorption of HDL particles by liver cells.
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