Catabolism of very-low-density lipoproteins in subjects with broad beta disease: comparison with endogenous hypertriglyceridemia.

The catabolic rates of VLDL apo-B from subjects with broad beta disease (type III hyperlipoproteinemia) and from subjects with endogenous hypertriglyceridemia (type IV hyperlipoproteinemia) were compared in recipients with these disorders. In subjects with broad beta disease, disappearance of autologous VLDL apo-B was slower than that of isologous VLDL apo-B from subjects with a type IV lipoprotein pattern (FCR 0.049 +/- 0.03 hr-1 for autologous vs. 0.068 +/- 0.035 for isologous, n = 6, p less than 0.05). However, the FCRs of autologous and isologous VLDL apo-B in subjects with type IV hyperlipoproteinemia were the same (0.110 +/- 0.051 hr-1 for autologous vs. 0.110 +/- 0.063 for isologous, n = 4, p = NS). In vitro studies suggested that 125I-VLDL from subjects with endogenous hypertriglyceridemia retained most of the smaller peptides (87.5% +/- 1.8 apo E and 75.7% +/- 1.6 apo C) when incubated with plasma from subjects with broad beta disease. By contrast, 125I-labeled IDLs from subjects with broad beta disease exchanged these lipoproteins rapidly (retaining only 7.9% +/- 0.03 apo-E and 8.2% +/- 0.3 apo-C) when incubated with plasma from subjects with endogenous hypertriglyceridemia. Similarly, beta-VLDL isolated from a subject with broad beta disease by preparative electrophoresis, when incubated with plasma from a subject with endogenous hypertriglyceridemia, exchanged its apo-E with the normal VLDL (56% being recovered in VLDL of alpha2 mobility). Normal VLDL, however, retained most (93.3%) of its VLDL apo-E radioactivity when incubated with plasma from a subject with broad beta disease. These observations suggest that the abnormal composition of autologous VLDL may in part be responsible for its delayed clearance in subjects with broad beta disease.