Glycation of plasma low density lipoproteins increases interaction with arterial proteoglycans

• Published in: Diabetes research and clinical practice 1999-10, Vol.46 (1), p.9-18
• Main Authors: Edwards, I.J., Wagner, J.D., Litwak, K.N., Rudel, L.L., Cefalu, W.T.
• Format: Article
• Language: English
• Subjects: Animals; Aorta, Thoracic - physiology; Aorta, Thoracic - physiopathology; Associated diseases and complications; Atherosclerosis; Biological and medical sciences; Diabetes; Diabetes Mellitus, Experimental - blood; Diabetes Mellitus, Experimental - physiopathology; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Glycation; Glycosylation; Humans; Kinetics; Lipoproteins, LDL - blood; Low density lipoproteins; Macaca fascicularis; Male; Medical sciences; Proteoglycans; Proteoglycans - metabolism; Reference Values
• ISSN: 0168-8227; 1872-8227
• DOI: 10.1016/S0168-8227(99)00074-1

The increased susceptibility to atherosclerosis of diabetic individuals, may result from diabetes-associated modification in plasma low density lipoproteins (LDL) which enhance their interaction with arterial extracellular matrix proteoglycans. Using a nonhuman primate model for human diabetes, studies were conducted to examine diabetes-induced changes in LDL. Plasma LDL were isolated from control ( n=4) and streptozotocin-induced diabetic ( n=3) cynomolgus macaques by differential ultracentrifugation. An in vitro binding assay was used to measure LDL interaction with arterial proteoglycans. Significantly more diabetic LDL bound to proteoglycans than control LDL (12.9±0.7 μg LDL cholesterol/μg proteoglycan versus 8.9±0.5 μg LDL cholesterol/μg proteoglycan (mean±S.E.M.), P