Topic
Very low-density lipoprotein
About: Very low-density lipoprotein is a research topic. Over the lifetime, 14491 publications have been published within this topic receiving 606996 citations. The topic is also known as: VLDL & Lipoproteins, VLDL.
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TL;DR: Apolipoprotein E is a plasma protein that serves as a ligand for low density lipoprotein receptors and, through its interaction with these receptors, participates in the transport of cholesterol and other lipids among various cells of the body.
Abstract: Apolipoprotein E is a plasma protein that serves as a ligand for low density lipoprotein receptors and, through its interaction with these receptors, participates in the transport of cholesterol and other lipids among various cells of the body A mutant form of apolipoprotein E that is defective in binding to low density lipoprotein receptors is associated with familial type III hyperlipoproteinemia, a genetic disorder characterized by elevated plasma cholesterol levels and accelerated coronary artery disease Apolipoprotein E is synthesized in various organs, including liver, brain, spleen, and kidney, and is present in high concentrations in interstitial fluid, where it appears to participate in cholesterol redistribution from cells with excess cholesterol to those requiring cholesterol Apolipo-protein E also appears to be involved in the repair response to tissue injury; for example, markedly increased amounts of apolipoprotein E are found at sites of peripheral nerve injury and regeneration Other functions of apolipoprotein E, unrelated to lipid transport, are becoming known, including immunoregulation and modulation of cell growth and differentiation
3,967 citations
TL;DR: Authors/Task Force Members (François Macha, Colin Baigentb,∗∗,2, Alberico L. Catapanoc), ESC Committee for Practice Guidelines (CPG) (Stephan Windeckeraa), ESC National Cardiac Societies (Djamaleddine Nibouchean, Parounak H. Patelcl)
2,972 citations
TL;DR: In this article, the authors quantified the biological sources of hepatic and plasma lipoprotein TAG in NAFLD patients, using stable isotopes for four days to label and track serum nonesterified fatty acids (NEFAs), dietary fatty acids, and those derived from the de novo lipogenesis (DNL) pathway, present in liver tissue and lipid TAG.
Abstract: Nonalcoholic fatty liver disease (NAFLD) is characterized by the accumulation of excess liver triacylglycerol (TAG), inflammation, and liver damage The goal of the present study was to directly quantify the biological sources of hepatic and plasma lipoprotein TAG in NAFLD Patients (5 male and 4 female; 44 ± 10 years of age) scheduled for a medically indicated liver biopsy were infused with and orally fed stable isotopes for 4 days to label and track serum nonesterified fatty acids (NEFAs), dietary fatty acids, and those derived from the de novo lipogenesis (DNL) pathway, present in liver tissue and lipoprotein TAG Hepatic and lipoprotein TAG fatty acids were analyzed by gas chromatography/mass spectrometry NAFLD patients were obese, with fasting hypertriglyceridemia and hyperinsulinemia Of the TAG accounted for in liver, 590% ± 99% of TAG arose from NEFAs; 261% ± 67%, from DNL; and 149% ± 70%, from the diet The pattern of labeling in VLDL was similar to that in liver, and throughout the 4 days of labeling, the liver demonstrated reciprocal use of adipose and dietary fatty acids DNL was elevated in the fasting state and demonstrated no diurnal variation These quantitative metabolic data document that both elevated peripheral fatty acids and DNL contribute to the accumulation of hepatic and lipoprotein fat in NAFLD
2,870 citations
TL;DR: Several indications exist that the acyltransferase reaction is the major source of plasma esterified cholesterol in man, and one possibility is that it plays a role in the transport of cholesterol from peripheral tissues to the liver.
2,336 citations
TL;DR: The cholesteryl Ester/Protein Complexes from Atherosclerotic Plaques and the Foam Cell in Familial Hypercholesterolemia are studied.
Abstract: PERSPECTIVES AND SUMMARY ............................... .... ....................................... 224 UPTAKE OF LIPOPROTEIN-BOUND CHOLESTEROL BY MACROPHAGES ................................................................................................ 226 Receptor for Acetyl-LDL .......................................................................................... 227 Receptor for LDLIDextran Sulfate Complexes ...................................................... 235 Receptor for f3-VLDL ,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,.,,,,,,,,.,,,,.,,.\", ... ,,,, .... ,, ............. ,,.............. 237 Receptors for Cholesteryl Ester/Protein Complexes from Atherosclerotic Plaques .............................................................. ,................... 241 PROCESSING AND STORAGE OF LIPOPROTEIN-BOUND CHOLESTEROL BY MACROPHAGES ............................... . ................................................ 243 Endocytosis and Lysosomal Hydrolysis .................................................................... 243 Cytoplasmic Re-esterification and Hydrolysis of Lipoprotein-Derived Cholesteryl Esters ........................................................................ \".\".\" . . . . . . . . . . .. . . . . . \".\".. 244 The Cho{estery{ Ester Cycle \" ... \" ... \" .... \" ....... \" .. \"....................................................... 247 SECRETION OF CHOLESTEROL AND APOPROTEIN E BY MACROPHAGES ........................................................................................ 249 Cholesterol Excretion Dependent on Cholesterol Acceptors .................................... 249 Synthesis and Secretion of Apoprotein E in Response to Cholesterol Loading , .. \"\", 252 IMPLICATIONS FOR FOAM CELL FORMATION IN ATHEROSCLEROSIS . . . . . . . . . . . . . . . . . ...... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..... . . . . . . . . . . . . . . . 255 The Foam Cell in Familial Hypercholesterolemia .................................................. 257
2,279 citations