High carbohydrate diets are known to increase the concentrations of very low density lipoprotein (VLDL) and to lower the concentrations of low density lipoprotein (LDL) and high density lipoprotein (HDL) in plasma. Such diets also alter lipoprotein compositions and metabolism. The aims of the present study were to assess in detail the effects of a virtually fat-free high carbohydrate (CHO) diet (CHO > 85% and fat < 1% of calories) on various aspects of LDL. Thirteen healthy normolipidemic volunteers ate a basal 'American' diet and the CHO diet for 7 days each in a forward or reverse sequence. Fasting blood samples were drawn at the ends of each study period and analyzed for lipoprotein lipid and apolipoprotein concentrations. Compositions of LDL particles isolated by ultracentrifugation were characterized chemically, LDL sizes were assessed by non-denaturing gradient electrophoresis on 2-16% gels, and association and degradation of LDL with normal human skin fibroblasts were quantified in cell cultures. Immunoreactivities of apoB in LDL were tested in solid phase competitive binding radioimmunoassays using five monoclonal anti-LDL antibodies that reacted with defined epitopes of apoB-100. The study diet produced consistent decreases of LDL cholesterol and apoB concentrations by 25% and 17%, respectively. LDL compositions were altered. Mean LDL triglycerides increased 3% to 4% of total LDL mass (P < 0.004), and LDL particle sizes decreased (P < 0.01). In radioimmunoassays that contained monoclonal antibody B1B3, an antibody that inhibits binding of LDL to the LDL receptor, the mean ED50 value for LDL protein was reduced from 3.75 to 2.66 μg (P < 0.001). Significant changes were not noted with the other four MAbs examined. In cell culture studies, CHO-LDL were associated with and degraded by human skin fibroblasts more avidly than basal LDL. Thus the ingestion of the high carbohydrate diet resulted in the appearance in plasma of LDL particles with a selectively modulated apoB-100 epitope near the LDL receptor recognition site and apoB-100. These LDL interacted more avidly with cultured human skin fibroblasts, which may explain in part the diet-related falls in plasma LDL concentrations.
|Number of pages||9|
|Journal||Journal of lipid research|
|State||Published - Jan 1 1989|