Diet and HDL Metabolism: High Carbohydrate vs. High Fat Diets

1987 
An increased level of plasma low density lipoproteins (LDL) is a major risk factor in the development of coronary artery disease (1). Conversely, plasma high density lipoproteins (HDL) and apolipoprotein A-I, the major protein constituent of HDL, are inversely related to the disease (2-4). In an attempt to reduce the incidence of heart disease, a number of organizations have suggested that dietary fat intake be reduced to 30% of calories (5). Since the protein intake of the U.S. population is approximately 20%, the resultant diet would result in an increase in dietary carbohydrate (CARB). Although high CARB diets reduce LDL-cholesterol, they also produce fasting hypertriglyceridemia, hyperinsulinemia (6) and decreased levels of HDL-cholesterol (6-8), all of which may be associated with increased risk of heart disease. Lipoprotein lipase (LpL) and hepatic triglyceride lipase are key enzymes in lipoprotein metabolism (9). LpL catalyzes the hydrolysis of chylomicron triacylglycerols and very low density lipoproteins (VLDL). The lipoprotein substrates for H-TGL are less well defined, although most evidence suggests that the enzyme plays a role in the catabolism of remnant lipoproteins (intermediate density lipoproteins) and in the degradation of HDL, particularly the HDL subfraction corresponding to HDL2.The purpose of the present study was to determine whether the effect of a high CARB diet on plasma lipids, and lipoproteins is correlated with changes in the activity of LpL and H-TGL. The results show that the dietary CARB-induced changes in HDL-cholesterol and HDL2, is significantly correlated to changes in LpL activity whereas H-TGL activity does not vary on a high CARB diet.
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