Chylomicrons are the preferred substrate for lipoprotein lipase in vivo

Triacylglycerol (TAG) enters the plasma from either exogenous (dietary) souces as chylomicron-TAG or from endogenous (hepatic) sources as very-low-density(VLDL) TAG. Most of the TAG is removed from these lipoproteins by lipoprotein lipase (LPL) of peripheral tissues, especially adipose tissue and skeletal muscle. The metabolic fates of these TAG-rich lipoproteins are not independent. In the fasting state VLDL is the major transporter of TAG. After a fat-containing meal there is an increase in plasma TAG which rises to a greater extent than can be accounted for by the appearance of chylomicron-TAG alone [l]. Some of this rise is due to an increase in particles containing apolipoprotein B100, presumably of hepatic origin [2]. Since insulin is known to inhibit hepatic VLDL secretion in vitro [ 3 ] it seems likely that the postprandial rise in VLDL-TAG reflects decreased clearance, perhaps because of competition for LPL by the postprandial influx of chylomicrons 141. This has not been directly investigated, neither have the relative roles of adipose tissue and skeletal muscle in the clearance of chylomicronand VLDL-TAG in the postabsorptive and post-prandial states. Nine healthy subjects (four female) were studied. Samples were taken from a vein draining the subcutaneous adipose tissue of the anterior abdominal wall, from an antecubital vein draining deep forearm tissue and from a vein draining a warmed hand (arterialised) or from a radial artery. Three sets of samples were taken after an overnight fast; the subject then ate a meal with an energy content of 3.1MJ, of