*Geek Box: Fat Metabolism
Fat metabolism can be complex, and the terminology even more so. So let’s run through it. Triglycerides are comprised of three fatty acids bound to a sugar compound, glycerol. Fat consumed through the diet is in the form of triglycerides, and when we store fat in the body it is also in the form of triglyceride: triglycerides can be thought of as storage lipids. When we consume fat, bile acids secreted by the gallbladder help to emulsify the triglycerides from diet, breaking them down into their component parts, which are taken up by intestinal cells and repackaged. Chylomicrons are very large compounds which transport triglycerides absorbed from diet to tissues, where they are broken down by the lipoprotein lipase [LPL] enzyme for energy, or stored.
However, we also release fats from storage, in the form of ‘free-fatty acids’ or ’non-esterified fatty acids’ [NEFA]: the liver can synthesise new triglycerides from circulating NEFA, and the liver produces very-low-density lipoprotein [VLDL] in order to transport these triglycerides [and also cholesterol] to tissues. So think of two pathways: exogenous [dietary] pathway with chylomicrons as the transporter for triglycerides, and endogenous pathway with VLDL as the transporter. It is important to note that a measure of triglycerides is not abstract, but a measure of the triglyceride content of chylomicrons, VLDL, and remnant lipoproteins. When the triglycerides in a chylomicron are broken down by LPL, it creates chylomicron remnants. When triglycerides in VLDL are broken down, it creates an ‘intermediate density lipoprotein’ [IDL], before further breakdown transcends IDL into LDL.
Thus, you can see how high triglycerides can influence cardiometabolic disease, by burdening the transport system. It is also why dietary factors that influence post-prandial triglyceride metabolism are important in the overall risk equation.