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25 Cards in this Set
- Front
- Back
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Chylomicrons
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Synthesised in the SI with ApoA and ApoB48
Mostly TG Largest ApoA, ApoB48, ApoCII, ApoE Deliver TG to tissues. LPL activated by ApoCII breaks the TG so the FA can ener the cell The left over chlosterol gets degraded in the liver by VLDL |
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VLDL
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Next largest Still a majority of TG but more protein
Synthesized in the liver from chylomicrons remenants FA (from glucose) and ApoB100 Also receivess ApoCII and ApoE Almost the same as Chylo just smaller |
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LDL
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Most chlosterol which it delievers to peripheral tissue
Synthesiszed in the blood derived from VLDL Still contains ApoB100 |
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HDL
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Contain ApoA as well as ApoCII and ApoE which it delivers to other and receives from other lipoproteins
Brings chlosterol from tissue back to liver "good" chlosterol Synthesized in liver and intestine |
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Situations when lipids are NOT carried on lipoproteins
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Low energy circumstances when TG are mobilizedfrom adipose as FA for energy and transported on ALBUMIN
MCFA and SCFA do NOT need to be carried on lipoprpteins |
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Apoproteins that are destined to be packaged with the cell into LP are synthesized where and then packed where?
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Synthesized in the RER and are packaged with lipids, chlosterol, and FS-Vit. in the Golgi
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ApoA
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Contained in HDL and Chylomicrons
Function: activate PCAT and ligand for HDL receptor |
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ApoB100
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LDL, VLDL, IDL
LDL receptor ligand Takes LDL into cells, need the extra part on the end |
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ApoB48
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Chylomicrons, chylo remanents
Chylo assembly and secretion, dietary lipids |
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ApoCII
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VLDL, HDL, Chylo
ACTIVATES LPL, transfers between HDL and VLDL/Chylo |
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ApoE
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VLDL, HDL, Chylo, Chylo remanents
Hepatic receptor ligand for chylo. Is recycled between HDL and VLDL/Chylo |
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What happens to gene to make ApoB48 vs. ApoB100
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RNA editing causes a change of CAA to UAA which is a stop codon
Taking a nitrogen off of cytosine CAA = ApoB100 UAA = ApoB48 |
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Chylomicron Remanents
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Made after LPL removes the FA and TG
Keeps ApoE because it is needed to attach to the liver liver combines these with new TG to make VLDL |
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LPL
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Insulin stimulates the synthesis
ApoCII activates it Diabetic pt. will NOT be able to store or use TG from lipoproteins |
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How do you get IDL vs. LDL
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Both from VLDL
TG = to chlosterol then IDL TG < then chlosterol LDL |
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LDL Rxn and regulation
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First step is to make HMG CoA from Acetyl Coa and Acetoacetyl CoA (KB) by HMG CoA synthetase
Next make Mevalonate by HMG CoA Reductase which is inhibited by high levels of chlosterol |
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ABCA-1
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Newly synthesized HDL are relatively lipid poor ApoA in HDL inreacts with this and ABCA-1 provides chlosterol to HDL from tissues
Makes it have its pancake shape |
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PCAT
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Carried by HDL
It converts chlosterol to chlosterol ester and fills up the HDL into a more round shape |
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CETP
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Bound to HDL it exhanges chlosterol esters on HDL for TG from VLDL
Deficiency results in higher HDL levels |
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PLTP
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It echanges TG on HDL for Phospholipids on VLDL
Deficiency results in lower levels of HDL and ApoA |
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What counteracts the oxidation of LDL in ECM?
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Vitamin E, C and Beta Carotene
If LDL builds up then it chances are increased to be oxidized into superoxidases which are then taken up by macrophages and turned into Foam cells which cause plaque |
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Statins
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Inhibit HMG CoA Reductase
Tissues stop making cholesterol Increased expression of LDL receptors which results in incresed remvoal of LDL |
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Nicotinic Acid/Niacin
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Increased HDL by blocking uptake by liver
Decreases mobilization of TG and decresed VLDL and LDL synthesis |
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Fibric Acid
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Decreased TG and Increased HDL
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Famial Hypercholesterolemia
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Addects synthesis/expression of of LDL receptors on cell
W/O them LDL can therefore cholesterol rises . Homozyhous is much worse then Hetero for this genetic disease |
