Metabolism of very low density lipoproteins in diet induced hypercholesterolemic pigtail monkeys (Macaca nemestrina).

Cholesterol-fed male pigtail monkeys were used to determine the metabolic mechanism of dietary hypercholesterolemia. Cholesterol feeding (200--400 mg/day) in monkeys produced a moderate hypercholesterolemia, which progressed with time and after 15 months the plasma cholesterol levels were raised 8-fold. The initial rise in plasma cholesterol was due to an increase in low density lipoproteins (LDL), but later the increases in intermediate (IDL) and very low (VLDL) density lipoproteins were mainly responsible for the rise in plasma cholesterol. To determine the metabolic mechanism, animals, both before and after cholesterol feeding, were co-injected with 131I-labelled VLDL from normal and 125I-labelled VLDL from cholesterol-fed donors. The fractional catabolic rate of autologous VLDL apolipoprotein B, which decayed biphasically, depended upon the dietary status of the recipient animal. The decrease in fractional catabolic rate was due to more VLDL apolipoprotein B being metabolized by the slower second phase. Normal VLDL apolipoprotein B in cholesterol-fed animals was catabolized by the slower second phase to a greater proportion than that in normal animals, where it was mainly transferred to LDL.