Metabolism of Apolipoproteins C-ll, C-lll, and B in Hypertriglyceridemic Men Changes after Heparin-induced Lipolysis

The C apolipoproteins are normally transferred to high density llpoprotelns (HDL) after lipolysis of very low density llpoproteln (VLDL) trlglycerlde. In previous studies, a loss of plasma C apolipoproteins was documented after heparin-induced lipolysis In hypertriglyceridemic subjects. The present studies were designed to determine If this decline In plasma C apolipoproteins was due to their clearance with VLDL remnants. Five Type IV hypertriglyceridemic and two normal subjects were Injected with I-VLDL and Mow density llpoprotelns (LDL) to document klnetically an excess of VLDL apollpoproteln (apo) B flux relative to LDL apo B flux In the Type IV subjects. A mean of 46% VLDL apo B was cleared from the circulation, without conversion to Intermediate density llpoprotein (IDL) or LDL. Heparln was then Infused (9000IU over 4 hours) to generate an excess of VLDL remnants that were not converted to IDL or LDL. VLDL trlglyceride, apo B, and apo C concentrations fell at a similar rate. VLDL apo B declined by 42% (p<0.01). However, no Increases were observed In IDL or LDL apo B In the Type IV subjects. This resulted in a 14% (p<0.01) decline In plasma apo B concentrations, Indicating a clearance of VLDL remnants. VLDL apo C-ll and C-lll concentrations fell by 42% (p<0.025) and 52% (p<0.01), respectively. During the first 2.5 hours of Infusion, they were almost quantitatively recovered In HDL Thereafter, the C apolipoproteins declined In HDL during which time VLDL apo C concentrations continued to decline. This resulted In a delayed fall (C-ll, 21%, p<0.025; C-lll, 26%, p<0.01) In plasma apo C concentrations. Thus, during enhanced lipolysis In Type IV subjects, C apolipoproteins were not cleared with VLDL remnants, but were initially transferred to HDL It Is possible that C apolipoproteins, along with VLDL surface llplds, form an HDL-like particle that Is destined for clearance rather than for recycling to newly formed VLDL (Arteriosclerosis 8:471-479, September/October 1988)