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Reverse cholesterol transport

Fig. 9.5 Forward and reverse cholesterol transport. Cholesterol is secreted by the liver in VLDL particles; these become LDL particles after hydrolysis of their triacylglycerol by lipoprotein lipase and hepatic lipase (see Fig. 9.3) and are taken up by tissues via the LDL receptor. A proportion of the particles will be taken up again by the liver. Cholesterol is removed from peripheral tissues by HDL particles via interaction with the receptor ABC-A1 (more details of HDL metabolism are in Fig. 9.4). This cholesterol is transferred to the liver by interaction with the receptor SR-BI and may be excreted in the bile. An alternative fate for the cholesterol in HDL particles is transfer via the action of cholesteryl ester transfer protein (CETP) to triacylglycerol-rich particles whose remnants thus become cholesterol-enriched. This is an alternative route for transfer of cholesterol to the liver. CE, cholesteryl ester; FC, free cholesterol.

has now become enriched with triacylglycerol. This HDL-triacylglycerol can be hydrolysed by hepatic lipase, leaving smaller, cholesteryl ester-depleted HDL3 particles which can then pick up further cholesterol from cells as outlined in the previous section.

In terms of defence against coronary heart disease this may sound a beneficial process. Unfortunately, things are not so simple. Some species - such as the rat - do not have CETP activity, and they do not suffer from atherosclerosis. Some families have been described in whom CETP is lacking; they have high HDL-cholesterol concentrations and appear to be protected against atherosclerosis. Probably the culprit is the cholesteryl ester-enriched remnant particle that results from CETP action. This will be considered again below (Section 9.4.3).

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