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Triglyceride-Rich Lipoproteins from Subjects with Type 2 Diabetes Do Not Demonstrate Increased Binding to Biglycan, a Vascular Proteoglycan

Departments of Medicine (L.R.T., K.L.O., A.C.) and Pathology (T.N.W.), University of Washington, Seattle, Washington 98195; Department of Medicine (P.H.R.B.), University of Western Australia, Perth 6001, Australia; and Hope Heart Institute (T.N.W.), Seattle, Washington 98104

Address all correspondence and requests for reprints to: Alan Chait, M.D., Box 356426, Department of Medicine, University of Washington, Seattle, Washington 98195-6426. E-mail: achait{at}u.washington.edu

Retention of atherogenic apolipoprotein (apo) B- and E- containing lipoproteins by their interaction with arterial wall proteoglycans is important in atherogenesis. Levels of triglyceride (TG)-rich lipoproteins, which contain both apo B and apo E, are increased in type 2 diabetes. Because increased retention of TG-rich lipoproteins in diabetes might explain, in part, the increased atherosclerosis in this disorder, TG-rich lipoproteins were isolated from fasting type 2 diabetic subjects and age-matched controls, and assessed for their ability to bind biglycan, a vascular smooth muscle cell-derived proteoglycan. The binding of TG-rich lipoproteins isolated from diabetic subjects to purified biglycan did not differ from lipoproteins isolated from control subjects. Moreover, contrary to previous reports, no difference in the apo E content of TG-rich lipoproteins was detected between the control and diabetic groups. Additionally, no difference in the binding affinity of TG-rich lipoproteins for the low-density lipoprotein receptor was observed between control and diabetic subjects. Thus, we were unable to confirm previous reports that TG-rich lipoproteins from subjects with diabetes are enriched in apo E compared with age-matched controls, consistent with the lack of difference in binding of these lipoproteins to either biglycan or the low-density lipoprotein receptor. Therefore, increased affinity of TG-rich lipoproteins for biglycan is unlikely to explain the increased atherosclerosis in type 2 diabetes.

This work was supported in part by Grants DK02456, DK07247, NCRR12609 from the NIH and a fellowship grant (to L.R.T.) from the Juvenile Diabetes Foundation. These studies were performed at the University of Washington’s General Clinical Research Center (Grant RR00037). The laboratory facilities and subject registry of the University of Washington Clinical Nutrition Research Unit (Grant DK35816) were used.

This paper was presented in part at the American Diabetes Association’s 60th Scientific Sessions, San Antonio, Texas, 2000.

Abbreviations: apo, Apolipoprotein; BMI, body mass index; FPLC, fast protein liquid chromatography; HbA1c, glycated hemoglobin; HDL, high-density lipoprotein; LDL, low-density lipoprotein; LDL-R, LDL receptor; MOPS, 3-(N-morpholino)propanesulfonic acid; TG, triglyceride; VLDL, very low-density lipoprotein.

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