PubMed · 10543041
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
N Shimazu. 1999. [Chylomicron].. https://pubmed.ncbi.nlm.nih.gov/10543041/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Postmenopausal estrogen therapy reduces cardiovascular morbidity and mortality, except in women with advanced coronary disease. This beneficial effect is partly attributed to a reduction of fasting plasma total and low-density lipoprotein cholesterol (LDL-C) and an elevation of plasma high-density lipoprotein cholesterol (HDL-C) concentrations. Since postprandial lipemia seems to play a role in the pathogenesis of coronary artery disease, we evaluated the effect of hormone replacement therapy (HRT) on postprandial lipoprotein metabolism in 14 normolipemic postmenopausal women. A vitamin A fat-loading test before and after three cycles of treatment with a sequential combination of conjugated equine estrogen (CEE) and medroxyprogesterone acetate (MPA) was used to label chylomicrons and chylomicron remnants with retinyl palmitate (RP), and RP clearance was assessed over an 8-hour period postprandially. Following 3 months of HRT, fasting total cholesterol and LDL-C levels were reduced 9.8% (P = .049) and 16.5% (P = .023), respectively. Fasting HDL-C levels increased 18.9% (P = .001). Fasting triglycerides (TGs) increased, but not significantly. Postprandial integrated plasma TGs did not change significantly. The integrated RP levels in whole plasma and chylomicron (Svedberg flotation units [Sf] > 1,000) and nonchylomicron (Sf < 1,000) fractions were reduced 58% (P = .043), 78% (P = .041), and 75% (P = .001), respectively, after hormonal treatment. Enhanced clearance of chylomicrons and chylomicron remnants by HRT may contribute to the protective effect of estrogens against cardiovascular disease in normolipemic postmenopausal women.
The lipid emulsions used in parenteral nutrition are constituted of particles rich in triacylglycerols (TAG) called artificial chylomicrons (200-500 nm in diameter; monolayer of phospholipids [PL] enveloping a TAG core) and PL-rich particles called liposomes (diameter inferior to 80 nm; bilayer of PL around an aqueous phase), which represent the excess emulsifier. Introduced into the circulation, the two populations of particles come into contact with circulating lipoproteins and cell membranes and experience the same overall fate: exchanges and transfers of lipids and apolipoproteins, enzymatic hydrolysis of TAG and PL, and internalization by different tissues. The relative importance of these different metabolic processes varies depending on the type of particle. The artificial chylomicrons undergo a hydrolysis of their TAG by lipoprotein lipase, with a release of fatty acids and formation of smaller particles of remnants, which are rapidly removed by the liver. In delivering fatty acids to the tissue, artificial chylomicrons fulfill an energy transport function similar to the natural chylomicrons. The liposomes hold little energy interest, and they also have deleterious effects when infused in excess. They inhibit the lipolysis of artificial chylomicrons and, by actively capturing endogenous cholesterol, they stimulate tissue cholesterogenesis and accumulate in the blood as lipoprotein-X, a long-lived abnormal lipoprotein. To limit as much as possible the metabolic perturbations due to the intravenous administration of exogenous PL, the emulsion has to be infused at a low rate, and should contain the minimal amount of excess PL.
Vitamins A and E differ in hydrophobicity. When added to a fat load more or less specific labeling of chylomicrons and their remnants can be expected and this allows to approach the mechanism of postprandial lipemia from a new sight of view. Applied in a study in which 20 patients participated (eight patients with familial dysbetalipoproteinemia (FD), six patients with familial combined hyperlipidemia (FCH) and six controls) we found that vitamin A, no longer paralleled the apo B-48 concentrations from 9 h after a fat load, especially in the remnant fraction with Sf 15-100. Qualitatively, the distribution of vitamin A to the more dense fractions mirrored that of vitamin E, but the latter was more rapid. Both vitamins at the maximum of remnant-accumulation, at 14 h after the fat load, correlated with the cholesterol content of the remnant fraction. For vitamin E there was a similar concentration dependent distribution to all other lipoprotein fractions. The results confirm our view that the lipoprotein mechanism can be regarded as a dynamic system. During regular episodes following the meals, exogenous fat is, like the vitamins, distributed over all endogenously formed lipoproteins. This transfer process results in the formation of beta-VLDL and contributes to the pathogenesis of FCH and FD.