Triglyceride:rich chylomicrons

Lipoprotein metabolism. Entero-cytes release absorbed lipids in the form of triglyceride-rich chylomicrons. Bypassing the liver, these enter the circulation mainly via the lymph and are hydrolyzed by extrahepatic endothelial lipoprotein lipases to liberate fatty acids. The remnant particles move on into liver cells and supply these with cholesterol of dietary origin. 

Fasted blood samples have to be analyzed for this analysis. When non-fasting samples are analyzed, the triglyceride-rich chylomicrons will be included in the VLDL fraction during this procedure, which will lead to false results. 

In an exogenous pathway, dietary cholesterol and triglycerides are absorbed by the gut enterocytes in the form of free cholesterol, fatty acids, and monoacylglycer-ols. Subsequently, the cholesteryl esters and triglycerides are incorporated into the triglyceride-rich chylomicrons and these processes involve several of the apolipopro-teins. The chylomicrons pass into the intestinal lymph system and then into the vascular circulation via the thoracic duct. Lipoprotein lipase (LPL) enables the transfer of fatty acids and triglycerides to the cells. Chylomicron remnants are transported to hepatic receptor sites. 

This approach can be used only for fat-soluble compounds that follow the same lymphatic route to be transported to the liver as carotenoids. The bioavailability of the compound of interest is determined by monitoring the appearance of the compound and its newly formed intestinal metabolites in the postprandial chylomicron fraction of plasma [also called the density < 1.006 kg/L fraction or triglyceride-rich lipoprotein (TRL) fraction because it is generally a mixture of chylomicrons (CMs) and very low density lipoproteins (VLDLs)] as a function of the time after ingestion. 

The liver requires cholesterol for synthesizing VLDL particles and bile acids. Triglyceride-rich VLDL particles are released into the blood and, like the chylomicrons, supply other tissues with fatty acids. Left behind are LDL particles that either return into the liver or supply extrahepatic tissues with cholesterol. 

TRL, triglyceride-rich lipoproteins that include VLDL and chylomicrons LDL, low-density lipoproteins HDL, high-density lipoproteins LPDP, lipoprotein-deficient plasma. b Significantly different from the corresponding preprandial value (p < 0.05). 

ApoA-IV is an immunologically distinct apolipoprotein of Mr 46,000 (B22, G28, W7). It has been demonstrated in intestinal epithelial cells from fasting subjects and a marked increase has been shown during lipid absorption (G27). About 10-13% of chylomicron apolipoprotein and 24-30% of intestinal VLDL apolipoprotein is apoA-IV. In fasting plasma, 98% of apoA-IV is in the d> 1.21 g/ml fraction and in lipemic plasma 90% is in this fraction, while 10% is associated with triglyceride-rich lipoproteins (G27). Gel permeation chromatography confirmed that in plasma most apoA-IV is free, unassociated with lipoproteins (B22, G27). 

Chylomicrons are triglyceride rich and contain apolipoprotein B-48 and the A types. The latter are synthesized in the intestinal tract cells. Additional apoproteins are transferred to the chylomicrons from HDL in circulation the apoE and apoC types. Their site of synthesis is the liver. The chylomicrons are subject to degradation by lipoprotein lipase in the peripheral tissue, especially adipose tissue. Lipoprotein lipase activity is increased by increased blood insulin levels. This enzyme is extracellular, attached to the capillary endothelial cells, and activated by ApoC-II, which is present in the chylomicrons. Lipoprotein lipase causes the hydrolysis of triglycerides, thus decreasing chylomicron size... 

Chylomicron triglyceride rich lipoprotein that transports... 

Chylomicron remnants and very low density lipoprotein (VLDL) remnants are rapidly removed from the circulation by receptor-mediated endocytosis. ApoE, the major apolipoprotein of the chylomicron in the brain, binds to a specific receptor and is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. Defects in apolipoprotein E result in familial dysbetalipoproteinemia, or type III hyperlipoproteinemia (HLP III), in which increased plasma cholesterol and triglycerides are the consequence of impaired clearance of chylomicron and VLDL remnants (Mahley et al., 1999). In the brain, lipidated apoE binds aggregated in a isoform-speciflc manner, apoE4 being much more effective than the other forms,... 

Although apoE was recognized first as a component of VLDLs (Shore and Shore, 1973 Shelburne and Quarfordt, 1974 Utermann, 1975 Kane et al., 1975), it has been demonstrated to be present in most other lipoprotein classes as well. In addition to occurring in the other triglyceride-rich lipoproteins, chylomicrons and their remnants, and the intermediate-density lipoproteins (IDEs), apoE is present in a subclass of the cholesterol-rich high-density lipoproteins (HDLs), referred to as HDL-with apoE (Mahley, 1978). By use of SDS-PAGE (Fig. 6), the Mr 34,200 apoE is easily distinguished from the other common apolipoproteins that also are present in the various human lipoprotein classes. 

Chylomicrons are synthesized in the intestine and transport dietary triglycerides and cholesterol. While circulating, the core triglycerides in these particles are hydrolyzed by lipoprotein lipase, which results in the production of a cholesterol-enriched remnant particle. When synthesized and initially released by the intestine, chylomicrons contain essentially no apoE, but as they circulate and are processed to remnants, the particles acquire apoE from other lipoprotein classes. This results in a shift of the distribution of apoE in plasma to the triglyceride-rich remnants in the absorptive state (Blum, 1982). 

Apoiipoproteins C-I, C-II, and C-III are associated with all lipoproteins except LDL. Apo C-I, the smallest of the C apoiipoproteins, has been reported to activate LCAT in vitro. Apo C-II plays an important role in the metabohsm of triglyceride-rich lipoprotein (VLDL and chylomicrons)... 

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