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Chapter: Introduction to Human Nutrition: Nutrition and Metabolism of Lipids

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Lipoprotein transport pathways - Circulating lipids: lipoprotein structures and metabolism

Lipoprotein transport can be described in terms of the production, transport, and removal of cholesterol or TAG from the circulation.

Lipoprotein transport pathways

 

Lipoprotein transport can be described in terms of the production, transport, and removal of cholesterol or TAG from the circulation. In reality, these two processes are inseparable because both TAG and cho-lesterol are transported together in lipoproteins. Lipoproteins are in a constant state of change, with lipids and apoproteins constantly shuttling between different lipoproteins that interrelate through inte-grated metabolic pathways. A useful analogy here is to think of lipoproteins as railway trains, transporting passengers that represent lipids and apoproteins within a complex rail network. The trains and passengers are in a constant state of flux within and between stations. Lipoprotein metabolism is con-trolled by the activity of functional proteins (enzymes, cell surface receptors, receptor ligands) that deter-mine the rate at which lipoproteins enter and leave the system, and by the physicochemical properties of the lipoprotein themselves. This corresponds to all of the rate-limiting features of a train journey, the number of trains, and type of passengers.

 All lipoproteins, with the notable exception of HDLs, begin life as TAG-rich particles The principal transport function of these lipoproteins in the first instance is to deliver fatty acids liberated from the TAG to tissues. The enterocytes in the gut are the producers of lipoproteins which deliver dietary fats into the blood as chylomicrons (exogenous lipid), whereas the liver is the central terminus for the pro-duction of VLDLs and removal of their cholesterol-rich end-products, LDLs. VLDLs, although smaller than chylomicrons, resemble the latter in many ways and are often referred to as the liver’s chylomicrons. While the rate at which the gut produces chylomi-crons depends largely on the amount of absorbed dietary fat, the rate of production of VLDL is deter-mined by the supply of fatty acids in the liver that can be re-esterified back to TAG for incorporation into VLDL. These fatty acids are derived chiefly from the systemic circulation in the form of nonesterified fatty acids (NEFAs), and to a lesser extent from the uptake of circulating lipoprotein remnants. It is noteworthy that, although the liver has the capacity to synthesize fatty acids, the amount synthesized by de novo lipo-genesis is relatively small in humans on a mixed Western diet. However, the contribution of fatty acids from this source may increase in conditions associ-ated with an overproduction of VLDLs, and has been shown to occur on low-fat, high-carbohydrate diets, and in metabolic disease.


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