Sobenin IA, Tertov VV, Orekhov AN
Int Angiol 1994 Mar 13:1 78-83

Abstract

Low density lipoprotein (LDL) from Type 1 and Type 2 diabetic patients, unlike LDL from healthy subjects, caused a 1.5- to 2.5-fold increase in the cholesterol content of cells cultured from unaffected human aortic intima, i.e. possessed atherogenic potential. LDL were further divided into two subfractions by affinity chromatography on Ricinus communis agglutinin-agarose. The amount of bound LDL was significantly higher in diabetic patients as compared with healthy subjects. Bound LDLs differed from unbound ones by significantly lowered sialic acid content, i.e. were desialylated lipoproteins. Desialylated, but not sialylated LDL subfraction induced massive cholesterol accumulation in cultured cells. Desialylated LDL subfraction in diabetic patients was also characterized by a higher degree of nonenzymatic glycation as compared to LDL subfraction with normal sialic acid level. Desialylated LDL had significantly decreased levels of free and esterified cholesterol, triglycerides and phosphatidylcholine and elevated amounts of lysophosphatidylcholine. These disturbances in lipid constituent of LDL were weak in healthy subjects, but conspicuous in diabetic patients. The results of this study have shown that there is in vivo modified LDL subfraction in the blood of diabetic patients which is characterized by crucial changes in protein and lipid moiety and are able to induce massive cholesterol accumulation in cultured cells.