In common with other long chain fatty acids, ALA which has been absorbed from the gut
passes into the circulation primarily esterified into TAG carried by chylomicron particles.
Chylomicron TAG are hydrolysed by lipoprotein lipase expressed on the endothelium;
adipose tissue lipoprotein lipase is upregulated in the post-prandial period which results in
targeting of meal fatty acids for storage. As a result of this TAG hydrolysis, TAG-poor
chylomicron remnants are formed. These are cleared from the circulation largely by hepatic
receptor-mediated uptake. The fatty acids from the chylomicron remnants are processed in
the liver and may re-appear in the bloodstream as components of TAG (in very low density
lipoproteins) or phospholipids. Through these processes ALA from the diet can be made
available to be incorporated into cell membranes and pools for storage (mainly in adipose
tissue), energy production (many cell and tissue types) or conversion to longer-chain ω-3
PUFAs (this is believed to mainly occur in the liver). The metabolic fates of ALA are
summarised in Figure 2 and each fate is discussed in further detail below.