These studies examine the mechanisms responsible for the heterogeneous nature of very low density lipoprotein (VLDL) triglyceride production. The fasting dog has been used as a model to follow the incorporation of [2-3H]glycerol and [1-14C]palmitate into the triglyceride of VLDL isolated from plasma and from mesenteric lymph. The former represents mainly hepatic VLDL, and the latter, intestinal VLDL. VLDL from each source has been subfractionated into Sf 100–400, Sf 60–100, and Sf 20–60 components. The plateau in triglyceride specific activity achieved during constant infusions of the labelled precursors was higher in small VLDL than in large VLDL. This indicates that the small VLDL triglyceride is not derived exclusively from that in large VLDL. This applies to both hepatic and intestinal VLDL. This contrasts with apolipoprotein B in small VLDL, which other studies show to be entirely derived from large VLDL. Thus both the liver and the intestine incorporate triglyceride into particles whose density extends through the entire VLDL spectrum. Unless triglyceride-rich lipoproteins with the density of VLDL but with no apolipoprotein B are produced, these data raise the possibility that triglyceride may enter VLDL directly.
Isopropanol precipitation method for the determination of apolipoprotein B specific activity and plasma concentrations during metabolic studies of very low density lipoprotein and low density lipoprotein apolipoprotein B.
