Alterations in levels and interrelations of plasma apolipoproteins induced by diet

Abstract

Diets high in carbohydrates increase the rates of hepatic secretion of VLDL in man. VLDL particles are secreted in greater numbers; they also tend to contain more triglycerides and to be larger in size. Comparable changes in intestinal secretion of chylomicrons and VLDL accompany fat absorption. We studied the metabolism of the ApoC apoproteins under these circumstances because in vitro studies suggest that these apoproteins may play important roles in the catabolism of VLDL. ApoA-I and ApoB were also examined because of their importance in HDL and VLDL structure, respectively. The fasting plasmas of 16 normolipemic young adults were examined before and after they had been fed high carbohydrate diets for 4–5 days. ApoA-I and ApoB were measured by radio-immunoassay. The relative proportions of ApoC-II and ApoC-III in VLDL were determined by disc gel electrophoresis. Lipids in plasma and in individual lipoproteins were determined chemically. Lipoproteins were isolated by ultracentrifugal and precipitation methods. VLDL-TG and VLDL-chol and VLDL-protein rose by factors of 2.4, 1.67, and 1.88, respectively. (Final value divided by initial value.) Since TG rose more than the others, VLDL became enriched by TG. LDL-chol fell by a factor of 0.78 while LDL-TG and LDL-ApoB remained constant, i.e., LDL became relatively enriched in TG and ApoB. HDL-TG rose by 1.42 and HDL-chol fell by 0.74, i.e., HDL too became TG enriched. Plasma ApoA-I fell by 0.84. Thus, there were alterations in both the levels and compositions of all lipoproteins. The proportion of ApoC-II relative to ApoC-III in VLDL increased in each subject on the carbohydrate diet (mean rise was 1.55-fold). The increases in ApoC were detectable after as little as 48 hr of diet, and the same results were obtained in two people who were each tested twice on two separate occasions several months apart. Thus, the changes in ApoC were reproducible. Proportions of ApoC-II were greater in S F > 400 than in S F 20–400 subfractions of VLDL on ad lib diets. Proportions of ApoC-II rose in both density subfractions on carbohydrate diets. The changes in both subfractions suggest that rises of ApoC-II in the total VLDL (S F > 20) fraction were not due solely to the accumulation of S F > 400 particles of unaltered ApoC composition in postdiet plasma. The changes following carbohydrate could have been due to secretion of altered lipoproteins or due to diet induced alterations in apoprotein catabolism. Three subjects were given 150 gm of corn oil to drink. Lipoproteins were analyzed, as above, at 0 and 3–12 hr after the drink. In spite of several-fold rises in the S F > 20 TG and proteins, the relative proportions of ApoC-II and ApoC-III remained constant. Thus, an acute dietary fat load and 2–4 days of carbohydrate diets provoked different responses. The fluctuations in the levels and relative proportions of ApoC support the notion that the ApoC group may have importance in vivo in the metabolism of VLDL.