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A B S T R A C T Smaller very low density lipoprotein (VLDL) remnants interact more readily with tissues than do larger "intact" VLDL. This may be related to changes in the availability of VLDL apoproteins on the surface of the lipoproteins. To test this hypothesis VLDL were incubated at 37°C with bovine milk lipase (LPL), and the abilities of LPL-treated VLDL preparations to compete with 1251-low density lipoproteins (LDL) for interaction with cultured normal human fibroblasts were measured. At the same time, the immunologic activities of these preparations were also tested by double antibody radioimmunoassay. Triglyceride (TG) contents of VLDL fell by 30-90% during incubation with LPL and, on zonal ultracentrifugation, VLDL of faster Svedberg unit of flotation (Sfl.063) rates (>150) were gradually converted to smaller VLDL with lower Sf rates (21-60).LPL-treated VLDL competed two to five times more effectively with 1251-LDL for binding to cellular receptors than did control VLDL. Control VLDL incubated with heat-inactivated LPL at 37°C, or with active LPL at 4°C had unaltered cell reactivities and TG contents compared with VLDL incubated without any enzyme. The direct uptake and degradation of LPLtreated VLDL was also assessed by using VLDL 125I1 labeled in apoprotein (Apo)B. LPL-treated VLDL-1251-ApoB were taken up and degraded by fibroblast at greater rates than were control VLDL-'25I-ApoB. Thus, hydrolysis of VLDL lipids was accompanied by an increased ability of VLDL to interact with fibroblasts. The immunoreactivity of ApoB in the same VLDL preparations, expressed as the "apparent ApoB contents" of LPL-treated VLDL, increased by 10-50% (P <0.02) in those assays that contained anti-LDL antisera, but the ApoB of control VLDL remained constant. However, assays that contained antisera directed against ApoB isolated from VLDL did not distinguish Received for publication 7 August 1978 and in revised form 9 July 1979. 1288 between LPL-treated and control VLDL. Thus, VLDL lipid hydrolysis was accompanied by changes in the immunoreactivity of VLDL-ApoB, which probably reflect changes in the disposition of ApoB on the surface of VLDL. The altered disposition of ApoB on VLDL "remnants" may be related to their enhanced interaction with cells.

Exercise can lower fasting triglyceride levels (TG). This study was undertaken to determine whether the exercise-induced decrease in TG is the result of a negative caloric balance. Five subjects with primary type IV hyperlipoproteinemia were given diets comparable in composition to their usual diets. During one experimental period the subjects exercised while maintaining their usual caloric intakes. During another experimental period their caloric intake was increased to compensate for the exercise-induced increase in energy expenditure. The exercise, which consisted of 30 min of treadmill walking per day for 4 days, resulted in a progressive decrease in TG. The reduction in TG, which averaged 120 mg/100 ml, occurred regardless of whether or not the increase in caloric expenditure was compensated for by an increase in food intake. The decrease in TG was limited to the very low density lipoprotein fraction. No significant changes occurred in total plasma cholesterol concentration or in the distribution of cholesterol between the lipoprotein fractions. Fasting plasma glucagon concentration was constant for each individual and was unaffected by the exercise. The finding that exercise induces a decrease in TG despite increased food intake indicates that the TG lowering effect of exercise is not mediated by a negative caloric balance.

Plasma high-density lipoprotein is commonly estimated by measuring the cholesterol remaining in plasma supernatant solutions after other lipoproteins, which contain apolipoprotein B, are precipitated with heparin and Mn2+. The method (method I) now in use by the Lipid Research Clinics, in which Mn2+ is at 46 mmol/liter final concentration, is reasonably accurate, but precipitation and sedimentation of lipoproteins other than high-density lipoproteins is often incomplete. We evaluated two modifications of method I. In method II, the Mn2+ concentration was doubled; the second modification (method III) included the increased Mn2+ concentration in a combined heparin Mn2+ reagent, decreased sample volume (2 ml), and a shorter incubation time (10 min at room temperature). The percentages of samples with turbid supernates (i.e., incomplete sedimentation) by methods I, II, and III were 9, 3, and 2%, respectively. Among non-turbid supernates, the percentages of samples containing measurable apolipoprotein B (incomplete precipitation) were 79, 19, and 16%, respectively. We conclude that method III is the most convenient and accurate of the three procedures.