The lipoproteins must deliver fatty nutrients to the tissues that need them, and then be removed from circulation (by the liver) when spent. The cycle is continual, with new nutrients entering into circulation by way of the liver, the skin, and many other tissues, on a continual basis. Major inputs come from the diet, and the ultimate disposal of broken-down fatty nutrients occurs with excretion into the bile. Because the flow of nutrients is continuous, the phases outlined below are broken into arbitrary points only for the sake of clarity.
The small intestinal cells manufacture the very first lipoprotein particles that newly ingested fats will circulate within, called chylomicrons. Chylomicrons enter the bloodstream via the thoracic duct, which bypasses the liver to dump directly into the left subclavian vein. Sometimes the term nascent chylomicron is used to describe the first lipoproteins particle manufactured by the intestinal cells. When nascent chylomicrons circulate through the bloodstream they encounter HDL and acquire certain marker proteins called apoproteins, some investigators prefer to describe chylomicrons as particles containing these apoproteins exchanged with HDL. (Because the science is in flux, the names are changing.) Chylomicrons circulate throughout the bloodstream for several hours distributing fatty nutrients to the tissues that are in need and receptive, and acquiring apoprotein markers from HDL.
Spent chylomicrons, also called chylomicron remnants, enter the liver carrying their new apoprotein markers presumably to identify them as non-foreign material, as well as to direct them into the correct section of the liver for further processing. The liver repackages useful fatty nutrients for the second phase of circulation, as well as adding some of its own newly manufactured or stored nutrients. The particle exits the liver with new apoprotein biomarkers, and at this point it is called Very Low Density Lipoprotein, or VLDL.
VLDL circulates through the bloodstream and, analogous to the process with chylomicrons, distributes fatty materials to the tissues that are in need and receptive. And just as with the chylomicrons, as they circulate they encounter HDL and acquire apoprotein surface markers. At this point the terminology becomes muddy. Some investigators describe the shrunken, spent VLDL particle as Intermediate Density Lipoprotein and others describe them as Low Density Lipoprotein. Again, the science is in flux and clouded by emotionality and a particularly unscientific set of assumptions, as the terms “good” and “bad” cholesterol suggest.
When dietary imbalances (such as low intakes of omega-3 fatty acids, excess intakes of hydrogenation made trans fats), smoking, vitamin deficiencies, genetic disease or other insult intervenes in the healthy role that plays the lipid cycle, some lipoprotein particles may start playing a deleterious role in health. Some may generate inflammatory processes at the endothelial lining of the blood vessels as well as inside the artery walls themselves. The extent and duration of an individuals inflammatory response, coupled with the underlying support strength of the vascular wall, determine whether the artery becomes scarred with atherosclerotic plaque, and determines the thrombotic potential of that plaque.
Many lipid scientists began their career with the understanding that cholesterol molecules are inherently dangerous and that the modern diet is unusually high in cholesterol, hence modern cardiovascular diseases are unusually prevalent among industrialized nations. As the science has become more sophisticated, we now understand that native cholesterol is not disease causing, and that oxidized cholesterol and other oxidized fats are the important class of fat-related factors, with other factors involved in atherosclerotic vascular disease being cigarette smoking, genetics, stress, and nutrient deficiencies, specifically low intakes of B-vitamins that allow a toxic agent, homocysteine, to be distributed by lipoproteins. However, the older belief that cholesterol is inherently bad still permeates the medical literature. This leaves us with a dichotomy of viewpoints and presents a significant barrier to progress in this field.
Textbook of Biochemistry With Clinical Correlations, Devlin. Fifth ed. Harrison’s Principles of Internal Medicine, 14th edition.