Insulin and triacylglycerol metabolism

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The enzyme lipoprotein lipase is activated in adipose tissue by insulin, as noted in previous chapters (see Section Thus, in the postprandial period, clearance of the triacylglycerol-rich lipoproteins is increased, and this increase in clearance occurs at the time of the peak triacylglycerol concentration in plasma, a few hours after a fatty meal. The removal of chylomicron-triacyl-glycerol is a saturable process, reflecting limited activity of lipoprotein lipase. After a fat-rich meal this pathway may become saturated. Both chylomicrons and VLDL compete for hydrolysis by lipoprotein lipase, a process that has been termed the common saturable removal mechanism. For reasons that are not entirely clear, lipoprotein lipase acts preferentially on larger particles, so chylomicrons tend to 'win'. One corollary of this competition is that the rapidity of clearance of excess triacylglycerol from the plasma in the postprandial period (i.e. after a meal) is dependent upon the subject's VLDL-triacylglycerol concentration: in someone with a low VLDL-triacylglycerol concentration, clearance of triacylglycerol after a meal tends to be more rapid. Because of the competition between chylomicron- and VLDL-triacylglycerol for hydrolysis by lipoprotein lipase, the VLDL-triacylglycerol concentration usually rises after a fatty meal (because its clearance is decreased).

It is beneficial to the individual to be able to clear excess triacylglycerol rapidly from the plasma after a meal (see Section 9.4.3, later). Thus, it makes sense for the body not to add extra VLDL-triacylglycerol to the plasma in this period. A number of studies of hepatocytes in vitro show that insulin suppresses VLDL output in the short term. These studies are difficult to perform in vivo, but in studies in which insulin has been infused into a vein, production especially of the larger, more triacylglycerol-rich VLDL particles is suppressed. In addition, the rate of VLDL-triacylglycerol secretion depends strongly on the delivery of non-esterified fatty acids from the plasma as a substrate for triacylglycerol synthesis. These are taken up by hepatocytes and esterified for secretion as VLDL-triacylglycerol. As we saw in Chapter 6 (Fig. 6.9), the concentration of non-esterified fatty acids in plasma falls after a meal due to suppression of adipose tissue lipolysis by insulin. On balance of the evidence, therefore, it seems likely that VLDL-triacylglycerol secretion is inhibited in the postprandial period.

There is an interesting parallel here with glucose metabolism following a meal. In both cases it seems that the body is 'buffering' the entry of substrates into the circulation. In the case of glucose, the entry of endogenous glucose (from hepatocytes) is suppressed after a meal, and the rate of clearance of glucose from the circulation is increased (mainly in skeletal muscle). Therefore the rise in blood glucose concentration is minimised. In the case of fat ingestion (at least when this occurs as part of a mixed meal, so that insulin release is stimulated) there is probably also a suppression of the entry of endogenous triacylglycerol into the circulation, and an increase in triacylglycerol clearance (mainly by adipose tissue). When this beautiful coordination breaks down, adverse consequences follow. In the case of glucose metabolism, failure of coordination leads to diabetes mellitus (Chapter 10). In the case of fat metabolism, it may lead to atherosclerosis (see Section 9.4.3).

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