Key result
TG-rich lipoproteins in T2D show no difference in biglycan or LDL receptor binding versus controls.
Why the study?
Do triglyceride-rich lipoproteins from subjects with type 2 diabetes demonstrate increased binding to biglycan compared to age-matched controls?
Observational
Do triglyceride-rich lipoproteins from subjects with type 2 diabetes demonstrate increased binding to biglycan compared to age-matched controls?
Increased affinity of TG-rich lipoproteins for biglycan is unlikely to explain the increased atherosclerosis observed in type 2 diabetes.
Answers are grounded in this paper and cite their sources.
Binding of TG-rich lipoproteins to biglycan does not differ in T2D; leaves open alternative mechanisms for accelerated atherosclerosis.
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.
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Tannock et al. (2002) conducted an observational in Type 2 diabetes. Type 2 diabetes vs. Age-matched controls was evaluated on Binding of TG-rich lipoproteins to biglycan. Triglyceride-rich lipoproteins from subjects with type 2 diabetes did not differ in binding to biglycan or LDL receptors compared with age-matched controls.
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