Triglycerides consist of three fatty acids that have reacted with glycerol.  Triglycerides and fatty acids are formed during digestive processes in animals. After a mammal ingests a fatty meal, the fats are acted upon by digestive secretions containing the enzyme lipase, which breaks down at least part of the triglycerides. The breakdown products and the remaining intact triglycerides then are absorbed through the intestinal cell wall and are recombined, at least in part, to form triglycerides and phospholipids. These lipids, in the form of very small droplets (chylomicrons), are transported in blood and in chyle (a milky fluid from the small intestine) to points of utilization or storage in the body.

One function of bile salts in digestion is to promote the linkage of (i.e., emulsify) lipid-soluble groups with water-soluble ones (such as those in enzymes) and also to increase the solubility of lipids in water. Both emulsification and solubilization are necessary because lipids are completely metabolized only at the lipid-water interface created by bile salts and by the salts of fatty acids (soaps), which are formed during the partial breakdown of lipids.

If an animal ingests more energy-rich substances (e.g., fats, carbohydrates) than it can utilize, excess fatty acids combine with glycerol to form neutral lipids, which are stored in the animal; e.g., in adipose tissue in mammals. If the energy requirements of the animal increase, the stored neutral lipids may then be broken down, each molecule forming three molecules of fatty acid and one molecule of glycerol. The three molecules of fatty acid combine with a protein (albumin) in mammalian blood plasma and are carried in the bloodstream to various tissues and organs that require energy. Neutral lipids probably also function as depots of concentrated energy in plant reproductive structures such as pollen grains and seeds; i.e., as food reserves for developing embryos.

The types of neutral lipids in an individual animal may vary according to the animal species and the composition of fats in the food it consumes. Fats used by or stored in animal tissues come from two sources—diet and enzymatic synthesis. The lipids synthesized from carbohydrates or proteins are characteristic of the animal species, whereas those resynthesized from dietary fats are characteristic of the food ingested. Many animals require some lipids containing one or more specific fatty acids, usually linoleic, linolenic, and arachidonic, to prevent the development of an essential fatty-acid deficiency, which is manifested by skin lesions, scaliness, poor hair growth, and low growth rates. These fatty acids cannot be synthesized by the animal and must be supplied in the diet.

Carbohydrates store only 4 KCal/g of energy, so fat stores over twice as much energy/gram as other sources of energy. Furthermore, lipids can be stored in an anhydrous form whereas carbohydrates typically cannot, which means that anhydrous lipid stores about 6 times as much energy per weight as hydrated carbohydrates. As an example, a typical 70 kg man would have to weigh approximately 125 kg if his energy stores were converted from triacylglycerol to glycogen.

Lipoproteins are conjugated proteins in which at least one of the components is a lipid.  They are held together not by chemical bonds, but rather by weak physical forces.  Lipoproteins are classified according to their densities and chemical qualities.  They are the principal means by which lipids are transported in the blood.  Many enzymes, transporters, structural proteins, antigens, adhesions, and toxins are lipoproteins.  All cells use and rely on fats, and for animals cholesterol is one such type of fat.  They are building blocks to create the multiple membranes which cell use to both control internal content, internal water soluble elements, and to organize their internal structure and protein enzymatic systems.  Lipoproteins in the blood, a water medium, carry fats around the body. The protein particles have charged groups aimed outward so as to attract water molecules; this makes them soluble in the salt water based blood pool. Triglyceride-fats and cholesterol are carried internally, shielded by the protein particle from the water.

Lipoproteins isolated from various sources usually fall into one of two general groups. In one group are the highly ordered lipoproteins, which are characterized by high protein and low lipid content; the other group consists of disorganized lipoproteins, which are characterized by low protein and high lipid content. A large number of different lipoproteins have been isolated; their molecular weights and lipid contents vary over a wide range. A suitable characterization of a lipoprotein includes several criteria; e.g., solubility characteristics, behaviour when spun in a centrifuge, and chemical composition.  Low density lipoproteins (LDL) have high lipid content.  The other group has high protein content and low lipid content (HDL).  Lipoproteins in blood—a water medium—carry fats around the body.  The proteins have a charged group which makes the molecule water soluble.  The triglyceride fats and cholesterol are carried internally.

High-Densithy Lipoproteins:  The metabolism of HDL is complex because of the multiple mechanisms by which HDL particles are modified in the plasma compartment and by which HDL particles are synthesized.  ApoA-I is the major HDL apoprotein, and its plasma concentration is a more powerful inverse predictor of CHD risk than is the HDL-level. 

Cellular synthesis:  When a cell requires cholesterol, it synthesises the necessary LDL receptors, and inserts them into the plasma membrane. The LDL receptors diffuse freely until they associate with clathrin coated pits.  LDL particles in the blood stream bind to these extracellular LDL receptors. The clathrin coated pits then form vesicles which are endocytosed into the cell.  The LDL particles arising from the catabolism of IDL have a half-life of 1.5 to 2 days.

After the clathrin coat is shed the vesicles deliver the LDL and their receptors to early endosomes, onto late endosomes to lysosomes. Here the cholesterol esters in the LDL are hydrolysed. The LDL receptors are recycled back to the plasma membrane.

LDL particles actually vary in size and density, and studies have shown that a pattern that has more small dense LDL particles—called "Pattern B"—equates to a higher risk factor for coronary heart disease(CHD) than does a pattern with more of the larger and less dense LDL particles ("Pattern A"). This is because the smaller particles are more easily able to penetrate the endothelium. "Pattern I", meaning "intermediate", indicates that most LDL particles are very close in size to the normal gaps in the endothelium (26 nm). 

Because of difficulty in acquiring the measurement of these two types of LDLs, these values are not routinely obtained.  Traditionally the cost difference was about 50 fold, though now through NMR spectroscopy this has changed; however, most commercial labs do not possess such equipment.  {Given the cost, side effects, and inconvenience of most drug treatments for high LDL, such measurement ought to be made, even thought it is not in the economic interest of the physician—jk}  There has also been noted a correspondence between higher triglyceride levels and higher levels of smaller, denser LDL particles and alternately lower triglyceride levels and higher levels of the larger, less dense LDL.  Reduction of triglyceride can be obtained by changes in diet and lifestyle and by medicinal doses of nicotinic acid--a fibrate is a secondary consideration. 

LDL liver pathway:  HMG-COA reductase inhibitors in the liver stimulate LDL receptors which results in an increased clearance from the liver of LDL.  Insulin induces HMG-COA, whereas glucagons down-regulates it.

Dietary: While glucagons production is stimulated by dietary protein ingestion, insulin production is stimulated by dietary carbohydrate.  The rise of insulin is generally determined by the unfolding of carbohydrates into glucose during the digestive process.  Glucagon levels are very low when insulin levels are high.  Lowering the blood lipid concentration of triglycerides (also known as VLDL) helps lower the amount of LDL, because VLDL is converted in the bloodstream into LDL.  A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism.  These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed with high fructose feeding in both humans and animal models.   Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic and intestinal overproduction of atherogenic lipoprotein particles.  Fructose the principle fruit sugar is widely used by the food industry in the form of high fructose corn syrup as a food sweetener.   [http://www.nutritionandmetabolism.com/content/2/1/5]

Risk reduction:  For reducing risk of cardiovascular disease, diet and lifestyle should be changed.  Reduce consumption processed sugars, fruit and sugars, saturated fats and trans fats.  Fill the dietary void with proteins and starches.  Avoid obesity and tobacco.  Avoid second-hand smoke and other sources of reactive chemicals such as in air pollution.  Exercise reduces risk--jk. 

Hyperlipoproteinemia

Hyperlipidemia, hyperlipoproteinemia or dyslipidemia is the presence of elevated or abnormal levels of lipids and/or lipoproteins in the blood. Lipids (fatty molecules) are transported in a protein capsule, and the density of the lipids and type of protein determines the fate of the particle and its influence on metabolism.  Abnormal levels of certain lipids, particularly cholesterol, triglycerides, and low-density lipoproteins are risk factors for atherosclerosis which elevates the risk for coronary heart disease and strokes.