The effect of short-term feeding of a high carbohydrate diet on HLD subclasses in normal subjects

Plasma HDL concentrations are effected by several perturbations, including certain dietary manipulations. In this study we have examined the effects of a one week ingestion of an isocaloric, fat-free, high-carbohydrate diet (CHO greater than 80% of calories) and the concentrations and compositions of plasma HDL subclasses. Eleven healthy normolipidemic volunteers (6 females, 5 males) took part in this study. Blood samples for lipoprotein analysis were drawn before and at the end of the dietary period and analyzed for lipoprotein lipid and apoprotein concentrations. Lipoproteins also were characterized by zonal ultracentrifugation. Our results show the following significant changes at the end of the dietary period: plasma concentrations of VLDL-TG, VLDL-cholesterol and total VLDL mass increased, whereas plasma concentrations of LDL-cholesterol, LDL mass and HDL-cholesterol and HDL mass, decreased. Plasma concentrations of apoprotein A1 decreased (from 133.3 +/- 7.7 to 108.1 +/- 8.6; mean +/- S.E.M., p less than 0.0004), and apoprotein A2 concentrations remained unchanged. This resulted in a drop in plasma ratio of ApoA1/ApoA2 (p less than 0.03). Since it has been shown that ApoA1/ApoA2 ratio is higher in HDL2 than HDL3, we examined the concentrations of these two subfractions, employing rate-zonal ultracentrifugation for their isolation. One week of ingestion of the study diet was followed by consistent decreases in HDL2 mass (from 84 +/- 15 to 44 +/- 16 mg/dl, mean +/- S.E.M.), with inconsistent changes in HDL3 mass, (from 254 +/- 18 to 222 +/- 13 mg/dl) resulting in significant decreases in HDL2/HDL3 mass ratio. Lipid analyses of these subfractions did not demonstrate major compositional changes. The alterations noted could be due to decreased HDL production, at least in part, but alterations in the interconversions of lipoproteins also could have played a role. The falls in HDL2 on a diet which should be "antiatherogenic" illustrate the difficulty of assessing the atherogenicity of any given diet solely by the changes it produces in the levels of circulating lipoproteins.