Primary and first passage aortic endothelial cells were shown to possess a high affinity receptor for beta-migrating very low density lipoproteins (beta-VLDL) distinct from the low density lipoprotein (LDL) receptor and scavenger receptor on these cells. In bovine aortic endothelial cells, 125I-rabbit beta-VLDL was taken up and degraded by a high affinity process that was competed for by unlabe...

We present an adolescent with McArdle disease and recurrent acute kidney failure due to rhabdomyolysis. The patient was admitted with acute kidney failure for 3 times and due to a history of proximal weakness, fatigue, and muscular cramps after physical activities a glycogen-storage disease was suspected. Serum creatine phosphokinase and urine myoglobin were found to be elevated. McArdle diseas...

fl-Migrating very-low-density lipoprotein (fl-VLDL) is a cholesteryl-ester-enriched lipoprotein which under normal conditions is rapidly cleared by parenchymal liver cells. In this study the characteristics of the interaction of,6-VLDL with rat parenchymal cells, Hep G2 cells and human parenchymal cells are evaluated. The binding of fl-VLDL to these cells follows saturation kinetics (Bmax respe...

BACKGROUND Currently the mechanisms of glomerular lipid accumulation are not completely understood. The present study characterizes the mechanisms of lipid uptake by glomerular cells. Since renal diseases are frequently associated with an accumulation of apoE-containing triglyceride-rich lipoproteins, we were interested to investigate whether glomerular epithelial or mesangial cells possess VLD...

Binding studies at 37 degrees C showed that lipoprotein lipase-treated very low density lipoproteins (LPL-VLDL) and very low density lipoproteins (VLDL), once taken up via the low density lipoprotein (LDL) receptor, are poorly degraded by HepG2 cells as compared with LDL. Determination of the initial endocytotic rate for LPL-VLDL and VLDL as compared to LDL shows that LPL-VLDL and VLDL are inte...

The in vivo fate of /3-very low density lipoproteins (0-VLDLs) was investigated after Cu-mediated oxidative modification (Ox-0-VLDL). Ox-0-VLDL may be physiologically relevant under conditions of defective VLDL removal by the liver (type HI hyperlipoproteinemia) or overloading of the remnant receptor (high cholesterol feeding). On oxidation of /3 -VLDL, the kinetics of its removal from the bloo...

The in vivo fate of beta-very low density lipoproteins (beta-VLDLs) was investigated after Cu(2+)-mediated oxidative modification (Ox-beta-VLDL). Ox-beta-VLDL may be physiologically relevant under conditions of defective VLDL removal by the liver (type III hyperlipoproteinemia) or overloading of the remnant receptor (high cholesterol feeding). On oxidation of beta-VLDL, the kinetics of its remo...

Murine P388D1 macrophages have a receptor pathway that binds human hypertriglyceridemic very low density lipoproteins (HTG-VLDL) that is fundamentally distinct from the LDL receptor pathway. Trypsin-treated HTG-VLDL (tryp-VLDL), devoid of apolipoprotein (apo)-E, fail to bind to the LDL receptor, yet tryp-VLDL and HTG-VLDL cross-compete for binding to P388D1 macrophage receptors, indicating that...