|  We measured hepatic CM remnant uptake in SD and in HN using [14C]cholesterol-labeled CM remnant. NIH Han S, Vaziri ND, Gollapudi P, Kwok V, Moradi H. Am J Transl Res. Hepatic [14C]cholesterol uptake was reduced in HN (69.3 +/- 6 vs. 7.2 +/- 2% of dose, P less than 0.001). We measured hepatic CM remnant uptake in SD and in HN using [14C]cholesterol-labeled CM remnant. This site needs JavaScript to work properly. Before being taken up by the liver, chylomicrons are hydrolyzed successively by two lipases. Chylomicron remnants are rapidly taken up into the liver (3, 14), carrying almost all … We measured hepatic CM remnant uptake in SD and in HN using [ 14 C] cholesterol-labeled CM remnant. Kinetic values were derived with multicompartmental models. The uptake of chylomicron remnants by the liver has been hypothesized to involve sequestration in the space of Disse, processing at the cell surface, and internalization by parenchymal cells via receptor-mediated endocytosis. Chylomicron remnants produced by lipolysis, are rapidly taken up by the liver via an apolipoprotein E (apoE)-mediated, receptor-dependent process. 4) Chylomicron remnants are removed from the circulation by the liver, mediated by apo E. Apo A, and Apo C are returned to the HDL molecules 5) One fate of cholesterol in the liver is incorporation into bile acids, which are exported to the intestine, completing the exogenous pathway cycle. 2. competent to bind to receptors. 2016 Jul;90(1):41-52. doi: 10.1016/j.kint.2016.02.026. Cigarette smoke alters chylomicron metabolism in rats. Endogenouscholesterol transport begins … TG uptake was reduced in HN measured kinetically (1.01 +/- 0.09 vs. 0.213 +/- 0.028 mg TG.min-1.100 g body wt-1, P less than 0.001) and reduced in all tissues (heart, skeletal muscle, fat, and liver). When a large portion of the triglyceride core has been hydrolyzed, chylomicron remnants are formed and are taken up by the liver, thereby also transferring dietary fat to the liver. Clinicians and clinical biochemists therefore recognize the need to measure TRL remnant lipoprotein levels in the fed and/or fasted state. Epub 2016 Apr 26. Notice the apoB48 and B100 apoproteins on the appropriate remnant. Chylomicrons are formed in the endoplasmic reticulum in the absorptive cells (enterocytes) of the small intestine. Wiley Online Library will be unavailable on Saturday 7th November 2015 from 10:00-16:00 GMT / 05:00-11:00 EST / 18:00-00:00 SGT for essential maintenance. These large, triacylglycerol-rich lipoproteins are CM remnants were increased significantly in plasma of HN. 1997 Nov;38(11):2173-92. The remnants then enter the liver cells where the protein is catabolized and the cholesterol released. Hepatic fatty acid and cholesterol metabolism in nephrotic syndrome. Get the latest public health information from CDC: https://www.coronavirus.gov, Get the latest research information from NIH: https://www.nih.gov/coronavirus, Find NCBI SARS-CoV-2 literature, sequence, and clinical content: https://www.ncbi.nlm.nih.gov/sars-cov-2/. Epub 2013 Mar 28. Elles sont responsables du transport des lipides exogènes de l'intestin grêle vers les tissus adipeux périphériques où ils sont retraités. The small circle at the top left represents a chylomicron remnant (CMR) and the one just below it is the remnant of VLDL called intermediate density lipoprotein (LDL). When LDLr is absent, remnants are taken up by a second apoE-dependent pathway, first to the sinusoidal space of the liver, with subsequent slow endocytosis and slow catabolism. We showed previously that proteinuria caused delayed chylomicron (CM) clearance in the rat and postulated the existence of a primary defect in CM hydrolysis. chylomicron remnant on the surface of the hepato- cytes [3]. Graded effects of proteinuria on HDL structure in nephrotic rats. Hepatic uptake of chylomicron remnants J Lipid Res. CM remnant uptake was significantly reduced in HN (58 +/- 1.2 vs. 20 +/- 0.86% uptake, P less than 0.01). The clearance of chylomicrons from the blood is rapid, the half-time of disappearance being under 1 h in humans. CM are catabolized on the vascular endothelium to atherogenic, cholesterol-rich remnant (CM remnant) particles, which are then rapidly taken up by the liver. Remnant lipoproteins are cholesterol-rich particles that are generated during circulation by lipolytic processing of liver-synthesized VLDL and intestine-synthesized chylomicrons (1, 2). This process liberates cholesterol, which is then either converted into bile acids, excreted in bile, or incorporated into lipoproteins originated in the liver (VLDL). The chylomicron remnants retain almost the whole of their original cholesterol content, which is cleared by the liver along with remnant … The line at the left in the illustration represents the hepatocyte membrane. chylomicron remnants (1, 2), which are derived from intestinal chylomicrons through the action of lipopro-tein lipase. Although CM remnant generation is impaired because of defective CM hydrolysis, the defect in hepatic CM remnant uptake is so severe that these particles accumulate in blood, posing a potential risk for atherogenesis. J Vasc Surg. Larger particles are catabolized more quickly than smaller ones. Apolipoproteins are significant in the synthesis and metabolism of chylomicrons. Chylomicrons are catabolized in the circulation by the lipoprotein lipase, which forms the chylomicron remnants. Triglyceride-rich lipoproteins as very low density lipoproteins and chylomicrons are snythesized by liver and intestine. [Article in French] Griglio S(1), Sultan F, Lagrange D. Author information: (1)Laboratoire de Physiopathologie de la Nutrition, Unité INSERM U 177, Paris, France. After uptake of chylomicron remnants by the liver, α-tocopherol stereoisomers are discriminated in the liver, and RRR-α-tocopherol (rather than SRR-α-tocopherol) is preferentially transported to each tissue. CM remnant uptake was significantly reduced in HN (58 +/- 1.2 vs. 20 +/- 0.86% uptake, P less than 0.01). 1992 Mar;41(3):325-33. doi: 10.2337/diab.41.3.325. We conclude that under normal circumstances, chylomicron remnants are rapidly internalized by LDLr and catabolized in hepatocytes, with a critical requirement for apoE. Copyright © 1992 the American Physiological Society, Copyright © 2020 the American Physiological Society, American Journal of Physiology-Renal Physiology, https://doi.org/10.1152/ajprenal.1992.263.2.F335, American Journal of Physiology-Cell Physiology, American Journal of Physiology-Endocrinology and Metabolism, American Journal of Physiology-Gastrointestinal and Liver Physiology, American Journal of Physiology-Heart and Circulatory Physiology, American Journal of Physiology-Lung Cellular and Molecular Physiology, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Journal of Physiology (1898-1976). The Scatchard analysis of the specific binding data showed a high affinity binding site for the remnants with a dissociation constant of 0.61 nM, assuming a molecular weight of 50 X 10(6) for chylomicron remnants. Chylomlcron remnant catabollsm appears to be mediated by apolipoprotein (apo) E binding to hepatic llpoprotein receptors. in the composition of the apoproteins on the surface of chylomicron remnants are the major determinants for hepatic recognition, a reduction in apoprotein C and an increase apoprotein E content are prerequisites for efficient remnant uptake by the liver'. [Role of hepatic lipase in the catabolism of chylomicron remnants in the rat]. Chylomicron remnant metabolism in human apolipoprotein E isoform-specific transgenic mice and the effects of apo E and Aß on the binding and uptake of remnant-like emulsions in Hep G2 cells The metabolism of chylomicron remnants in mice deficient in low density lipoprotein receptor (LDLr) or apolipoprotein E (apoE) was compared with that of control C57BL/6J mice. Lipoprotein lipase (LPL) on endothelial cell surfaces in capillaries and, to a lesser extent, hepatic lipase (HL) in the liver hydrolyze the triglycerides of these … CM are catabolized on the vascular endothelium to atherogenic, cholesterol-rich remnant (CM remnant) particles, which are then rapidly taken up by the liver. Chylomicron remnant and asialoglycoprotein metabolism are independent. ABSTRACT Chylomicron catabolism is known to be initiated by the enzyme lipoprotein lipase (triacylglycero-protein acyihydrolase, EC 3.1.1.34). Clinical and experimental evidence suggests that chylomicron and VLDL remnants, i.e., triglyceride-rich lipoprotein (TRL) remnants, play a significant role in the onset and development of atherosclerosis. Contraceptive steroids increase hepatic uptake of chylomicron remnants in healthy young women. Chylomicron and chylomicron remnant metabolism in STZ-induced diabetic rats. The remnants rapidly enter the liver by receptor-mediated endocytosis after binding to spe-cific remnant receptors (3-5). We conclude that under normal circumstances, chylomicron remnants are rapidly internalized by LDLr and catabolized in hepatocytes, with a critical requirement for apoE.  |  It is possible that apoE-2 may have an inhibitory effect on lipolysis of chylomicronssimilar to that described for the conversion of P-VLDL to LDL by Ehnholm et al. Subsequent analysis has demonstrated that the LRP is present in a variety of tissues, including liver, kidney, placenta, and brain. Thus the nephrotic syndrome causes a primary defect in the uptake of TG from CM that is expressed in all tissues and a separate defect in hepatic CM remnant uptake. In 1988, this remnant receptor was cloned and dubbed the LDL receptor-related protein (LRP). COVID-19 is an emerging, rapidly evolving situation. [Role of hepatic lipase in the catabolism of chylomicron remnants in the rat]. 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