Warning:
JavaScript is turned OFF. None of the links on this page will work until it is reactivated.
If you need help turning JavaScript On, click here.
The Concept Map you are trying to access has information related to:
Lipoproteins, -formed from sequential LPLing of IDL -contains only ApoB100 -high [CE], [cholesterol] -thus main atherogenic Lipoprotein -MAJOR PLASMA CHOL. CARRIER -cleared by liver DM->glycosylated, so no uptake by LDLR LDLs I-IV LDL IV-highest density, atherogenicity LDL I-highest affinity for LDL receptor, Neutral Chol. Ester Hydrolase (NCEH) -hydrolyzes pool of CEs in cytosol Into HDL ApoA-I interacts w/ ABCA1 on plasma memb. -delivers chol to ApoA-I, forms nascent HDL -ABCG1 delivers chol to HDL, not ApoA-I -also, chol. could efflux from PM via diffusion, Lipoproteins Apolipoproteins Bind, emulsify lipids Ligands for receptors for uptake(B, E) Cofactors for enz. metabolism(A-I, C-II), **Transport exogenous (dietary) TGs & Vitamins A,D,E,K -packaging of TGs in enterocyte Largest, Least dense, Highest lipid:pro Contains ApoB48, C-II, C-III Synth-lipids in sER, proteins in rER -assemble in Golgi Nascent w/ only ApoB48, A-I, A-IV -secreted via exocytosis into lymph -C-II, C-III, E from HDL Fate Lipoprotein Lipase(LPL)-along endoth walls -hydrolyze some TG->FFAs -oxidized in mm. for energy and stored -stored as TGs in adipocytes -made by adipose tissue, mm. (cardiac), mamm. gland -transported to cap. endoth, anchor by hep. sulfate -activated by C-II, inhibited by C-III Upregulated by insulin, Diet:for dietary-induced variety -limit chol, sat'd fat in diet Drugs-Together, reduce LDL by 50-75% Chol. absorption inhibitors Ezetimibe (Zetia), eg. Block NPC1L1 sterol transporter -moves chol from intestinal lumen to enterocytes NL absorption of FAs, TGs, bile acids, vitamins lower side effects than statins -used in combo w/ statins (Vytorin), Forward-from liver/intestines to periph Reverse-Periph to liver/steroidogenic cells -only these can catabolize cholesterol Chol. homeostasis to maintain FREE CHOL. in cells NPC1 NPC1 facilitates transport of chol to PM, ER (ACAT activated and CEs formed in ER) Niemann-Pick type II-autosomal Recessive 1:100K live births, Fr. Acadian-1:100 -mutation in NPC1 gene -hepatosplenomegaly -lysosomes accumulate chol. -ataxia, progressive dementia, -formed from sequential LPLing of IDL -contains only ApoB100 -high [CE], [cholesterol] -thus main atherogenic Lipoprotein -MAJOR PLASMA CHOL. CARRIER -cleared by liver DM->glycosylated, so no uptake by LDLR LDL Receptor -means of cell uptake of LDL -(-)charged glycoproteins in coated pits -ApoB100+LDLR->internalization of complex -vesicles fuse to form endosomes -lower pH, so LDL dissociates from receptor -LDLRs recycled to plasma memb. -LDL degraded by lysosomal enzymes -Chol, AAs, FAs, phospholipids released, Hyperlipidemias-circulating chol, TGs high Tx Diet:for dietary-induced variety -limit chol, sat'd fat in diet Drugs-Together, reduce LDL by 50-75%, Lipoproteins Chylomicrons **Transport exogenous (dietary) TGs & Vitamins A,D,E,K -packaging of TGs in enterocyte Largest, Least dense, Highest lipid:pro Contains ApoB48, C-II, C-III Synth-lipids in sER, proteins in rER -assemble in Golgi Nascent w/ only ApoB48, A-I, A-IV -secreted via exocytosis into lymph -C-II, C-III, E from HDL, ApoA-I interacts w/ ABCA1 on plasma memb. -delivers chol to ApoA-I, forms nascent HDL -ABCG1 delivers chol to HDL, not ApoA-I -also, chol. could efflux from PM via diffusion Inside HDL ApoA-I activates LCAT, free chol->CE when full of CE->'HDL2' w/ VLDL/LDL, exchange CE for PL, TGs -via CETP HDL2 hydrolyzed by hepatic lipase ->HDL3 - TG-poor, cleared by kidney HDL can be removed by liver