Bile salts density

Dextrothyroxine speeds up the decomposition of cholesterol and lipoproteins, thus activating catabolism of cholesterol in the liver, which results in cholesterol being more intensively transformed into bile salts. It lowers the level of low-density lipoproteins in the plasma and very low-density lipoproteins in fatty tissue. It is recommended for treating hyperlipoproteinemia. Synonyms of this drug are choloxin, lizolipin, natexin, travenon, and others. 

The fourth major lipoprotein type, high-density lipoprotein (HDL), originates in the liver and small intestine as small, protein-rich particles that contain relatively little cholesterol and no cholesteryl esters (Fig. 21-40). HDLs contain apoA-I, apoC-I, apoC-II, and other apolipoproteins (Table 21-3), as well as the enzyme lecithin-cholesterol acyl transferase (LCAT), which catalyzes the formation of cholesteryl esters from lecithin (phosphatidylcholine) and cholesterol (Fig. 21-41). LCAT on the surface of nascent (newly forming) HDL particles converts the cholesterol and phosphatidylcholine of chylomicron and VLDL remnants to cholesteryl esters, which begin to form a core, transforming the disk-shaped nascent HDL to a mature, spherical HDL particle. This cholesterol-rich lipoprotein then returns to the liver, where the cholesterol is unloaded some of this cholesterol is converted to bile salts. 

The data clearly indicate that the surface pH of the bile salt micelle is higher than the surface pH of a lauryl taurate micelle for a given bulk pH—i.e., the difference between bulk and surface pH is less with the bile salt micelle. The bile salt micelle should have a lower charge density and therefore a lower concentration of protons at the surface of the micelle. Therefore, the observed bulk pH at which micellar fatty acid ionizes is closer to the bulk pKa of molecularly dispersed fatty acid (4.9) in bile salt solution than in lauryl taurate solution. 

Recently the means by which pectin lowers cholesterol levels and even the validity of this effect have been questioned. Upon finding no bile salt binding capacity for soluble pectin, Baig and Cerda (76) proposed that pectin lowered serum cholesterol levels by forming insoluble complexes with the serum low density lipoproteins (LDL) which transport circulating cholesterol. Complexing of LDL by citrus pectin was observed in vitro, but the way in which pectin or some component thereof enters the blood stream to effect such binding in vivo has not been determined. 

Abbreviations GcL, Geotrichum candidum lipase hPL, human pancreatic lipase RmL, Rhizomucor miehei lipase hHL, human hepatic lipase hLPL, human lipoprotein lipase hLAL, human lysosomal acid lipase hGL, human gastric lipase BAL, bile salt-activated lipase HSL, hormone-sensitive lipase CLP, colipase AChE, Torpedo cal omica acetylcholinesterase cDNA, complementary deoxyribonucleic acid VLDL, very low-density lipoprotein IDL, intermediate-density lipoprotein HDL, high-density lipoprotein apoC-II, apolipoprotein C-II. 

About 80% of the cholesterol synthesized in the liver is converted into bile salts. The remainder of the cholesterol, triacylglycerols, other lipids, and hydrophobic substances (including xenobiotics) are transported to other tissues throughout the body by plasma lipoproteins. These lipoproteins, which are classified according to density, consist of apoproteins (also made by the liver) and various combinations of fat and fat-soluble compounds. The liver also stores vitamins, especially vitamin A but also vitamins D, E and K, as well as vitamin B12, in fatstoring Ito cells, located between endothelial cells and hepatocytes. 

Cholesterol is obtained from the diet and synthesized in most cells of the body. It is a component of cell membranes and the precursor of steroid hormones and of the bile salts used for fat absorption. High concentrations of cholesterol in the blood, particularly the cholesterol in lipoprotein particles called low density lipoproteins (LDL), contribute to the formation of atherosclerotic plaques. These plaques (fatty deposits on arterial walls) are associated with heart attacks and strokes. A high content of saturated fat in the diet tends to increase circulatory levels of LDL cholesterol and contributes to the development of atherosclerosis. 

Cholesterol is packaged in chylomicrons in the intestine and in very-low-den-sity lipoprotein (VLDL) in the liver. It is transported in the blood in these lipoprotein particles, which also transport triacylglycerols. the triacylglycerols of the blood lipoproteins are digested by lipoprotein lipase, chylomicrons are converted to chylomicron remnants, and VTDT is converted to intermediate-density lipoprotein (IDL) and subsequently to low-density lipoprotein (LDL). These products return to the liver, where they bind to receptors in cell membranes and are taken up by endocytosis and digested by lysosomal enzymes. LDL is also endocy-tosed by nonhepatic (peripheral) tissues. Cholesterol and other products of lysosomal digestion are released into the cellular pools. The liver uses this recycled cholesterol, and the cholesterol that is synthesized from acetyl CoA, to produce VLDL and to synthesize bile salts. 

An elevated plasma concentration of cholesterol (in low-density lipoproteins) is a risk factor for atherosclerosis and ischaemic heart disease. As discussed in section 7.3.2.1, the dietary intake of cholesterol is less important as a determinant of plasma cholesterol than is the intake of total and saturated fat, or the intake of compounds that inhibit the reabsorption of cholesterol secreted in bile, or the reabsorption of bile salts themselves (section 4.3.2.1). 

Other Lipids. Other important lipids include primarily the phospholipids, lipoproteins, and cholesterol. All cells contain phospholipids. They are structural compounds found in cell membranes and in the blood. The brain, nerves, and liver contain particularly high levels. Lecithin is one of the most abundant phospholipids in the diet and the body. Phospholipids are powerful emulsifying agents. Lipoproteins are the primary vehicle for lipid transport in the blood. There are four main types chylomicrons very low density lipoproteins (VLDL) low density lipoproteins (LDL) and high density lipoproteins (HDL). Cholesterol is derived from the dietorsyn e-sized in the body. It is necessary for the formation of hormones and bile salts. These will all be discussed in sections which follow. 

The effect of addition of a bile salt, sodium deojqrcholate (NaDC), on the morphology transition in aqueous cetyl trimethylammonium bromide (CTAB) has been studied. Visual, optical density and zero-shear viscosity data of the aqueous mixtures provide some basic macroscopic information on phase behavior. NMR spectra show the peak broadening on increasing the [NaDC] in the system confirming the presence of a mixture of micelles and vesicles. ... 

Because there were no pubUshed reports of the local effects of vitamin E on the periarticular tissue, it is necessary to determine local toxicity using animal studies. Tocopherols that are orally from food or supplements are transported across the gastrointestinal membrane by passive diffusion after solubilization by mixing with chyme and bile salts in the stomach and small intestine [8]. Tocopherols are then incorporated in chylomicrons, which are taken up by the liver. After secretion from the liver, low density lipoproteins (LDLs) and high density lipoproteins (HDLs) are the major carriers of tocopherols in humans [101]. 

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