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45 Cards in this Set

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What is cholesterol?
-4 ring structure
-has an OH at the 3' position
-has a bit of a hydrocarbom chain
Properties of cholesterol, where is it found?
-Found in biological mb
How is cholesterol made?
From acetyl CoA or acetate
*Note all the lipids (phospholipids, sphingolipids etc) and cholesterol are mae from acetyl CoA
What are the steps of cholestrol synthesis?
1)Combine 2 acetyl CoAs
2)Add 3rd acetyl CoA to form HMG-CoA, using HMG CoA synthase
3) HMG-CoA Reductase, reduce HMG-CoA to Mevalonate
4)Series of P using ATP to convert Mevalonate (6C) to Isoprene (5C)
5)Synthesize Geranyl (10C), Farnesyl (15C), Geranyl-Geranyl (20C) starting with isoprene (5C)
6)Squalene synthase is used to synthesize squalene (30C) from 2 Farnesyls
7) 3 decarboxylations to produce cholesterol (27C) from squalene
What is the rate limiting enz in cholesterol synthesis?
Which drugs target it?
-HMG-CoA Reductase
-Statins target it
What can isoprene and its subsequent products be used to build?
-Gernayl (10C)
-Farnesyl (15C)
-Gernaylgeranyl (20C)
-Squalene (30C)
Why would you target squalene synthase over HMG-CoA reductase?
Reduce side-effects cuz farnesyl/geranylgeranyl are used as hydrophobic anchors/tags for ptn. If you inhibit HMG-CoA reductase, don't make these products but if you inhibit Squalene synthase, make them and don't get side effects
What are some derivatives of the cholesterol path/isopropene units?
Vitamin A
Vitamin K
What can cholesterol be converted to?
-Ble acids
-Vitamin D
-Steroid hormones:progesterone, testosterone, estradil aldosterone, cortisol
What are statins?
-Inhibitors of HMG-CoA reductase
-resemble mevalonate and are .: competitive inhib. of HMG-CoA reductase
How are cholesteryl esters formed?
By PC + cholesterol, through the action of LCAT (transfers fatty acyl gp from PC to cholesterol)
What are cholesteryl esters used ofr?
Storage form of cholesterol cuz its no lonnger amphipathic. Stored in the same area as triacylglycerols
Cholesterol formation in the cell?
Combine Acyl CoA and cholesterol. Use ACAT to transfer acyl group from acyl CoA to cholesterol to fomr the cholesteryl ester and CoA
What is the difference between ACAT and LCAT?
ACAT: in the cell. gets its acyl group from Acetyl CoA
LCAT: in the plasma. gets its acyl group from PC
Important points about cholesterol.
-Very stable: no enzymes can degrade cholesterol, only convert it
-small amounts used for steroid hormnes, bile acids, vitamins, isoprenes etc
-important in bio. mbs
-plasma mb where most of cholesterol located
-can be converted to cholesteryl ester for storage
-can be converted to vitamin D
Differences between cholesterol and bile acids?
-Bile acids have many more OH gps and are more hydrophilic
-They help emulsify fats
How do you target proteins?
Target protein to a mb by making thm very hydrophobic.
i.e.: add fatty acyl group of farnesyl/geraylgeranyl gp
What is HMG-CoA reductase ?How is it regulated? (Inhibitors/activators)
-Rate limiting enz of the cholesterol synthesis path
-Inhibitors: Glucagon, cholesterol (also stimulates ACAT to make cholesteryl esters to be stored in lipid droplets)
-Activators: Insulin
What are two ways to get cholesterol into the cell?
1) Make it in the cell (using ACAT)
2) Endocytosis of cholesterol carrying poteins (LDL)
What is a lipoprotein?
Complex of phospholipid, ptns, cholesterol and sometimes FA
What are lipoproteins used for?
Carriers of cholesterol
How are cholesterol transported?
1)Cholesterol is present in LDL (;cholesterol carrier) in the form of cholesteryl ester
2) LDL binds the LDL receptor
3)This complex is engulfed when the invaginates, forming a clathrin coated pit (Receptor mediated endocytosis)
4)LDL is separated from the LDL receptor so that it can be recycled to the cell surface
5)LDL is degraded inside the lysosome (everything inside is degraded to its basic subunits, except cholesteryl ester which is only degraded to cholesterol, which cannot be further degraded)
6)Cholesterol is transported to the ER mb
Three regulatory steps when cell needs cholesterol?
1)Express LDL receptor
2)Make cholesterol (express more HMG-CoA reductase)
3)Liberate cholesterol from lipid droplet
Three regulatory steps if cell has too much cholesterol?
1)Stop making LDL receptors and reduce them if possible
2)Stop making HMG-CoA reductase (degrade if req'd)
3)Store cholesterol as cholesteryl ester in the lipid droplets
How is cholesterol regulated?
-On the basis of SCAP and SREBP binding
-SCAP has a STEROL sensing domain (SSD)
-When SCAP binds cholesterol, it bind to SREBP.
-If no cholesterol, SCAP does not bind SREBP and SREBP is free to go wherever it wants.
What happens when there is no cholesterol in the cell?
-No cholesterol in the cell then no cholesterol in the ER mb.
-SCAP doesn't bind SREBP .: it is free to go to the golgi through a secretory mechanism
-In the golgi, SEBP is cleaved by 2 proteases, forming a soluble ptn
-Soluble ptn gos to nucleus and acts as a TF
-Stimulates LDL receptor an HMG-CoA reductase
What happens when cholesterol lvl in the cell is high?
-SCAP binds cholesterol
-This binding prevents release of SREBP .: it can't go to the golgi or nucleus and it can't upregulate the target genes, .: won't actto increase transcription of cholesterol
How can you regulate cholesterol lvls in the cell?
-Mb of ER (using SCAP and SREBP)
3 shapes of phospholipids?
-Micelle (hydrophobic interior)
-Liposome (core is water, has a bilayer)
*most organelles are liposomes
What are the components of the mb? Why do the component proportions vary?
-Protein, phospholipids, sterols
-Composition varies depending on how stiff/fluid you want the mb to be
Which has higher affinity for cholesterol: sphingolipids or phospholiids?
What are lipoproteins composed of?
Proteins, phospholipids, free cholesterol, cholesteryl esters and triacylglycerols
How do you separate diferent lipoproteins from each other?
Density ultracentrifugation
(Fattest one float to the top and least fat ones sink to the bottom)
What is the order of density of the different lipoptns?
Chylomicron< VLDL<LDL<HDL
-lower the density, higher the concentration of TAG, lower the concentration of ptn
Which organ regulates the body's cholesterol metabolism?
What are the steps of the forward cholesterol path (path from diet to liver to tissues)?
1)Chylomicron containing CE and TG, has intergral ptn Apo-B48. As it travels through the the blood, it is acted on by lipases: releases FFA.
(the Remnant is wtv is left of the chylomicron, but it still contains CE and Apo-B48)
2) Apo-E binds remnant receptor on the liver and mediates endocytosis of the remnant
3)Once FC and CE in theliver, can package it into VLDL (has Apo-B100)
4)The VLDL has FFA, TG and CE in it. As it travels through the blood, it is acted on by lipases, releasing FFA=> lef with another remnant: LDL
5)LDL only has CE in it. LDL interacts with the LDL receptor of a cell, via Apo-B100
=>mediates endocytosis to release FC and CE inside the cell
What happens when cells have too much cholesterol?
-Cells downregulate LDL receptor
--If all cells downregulate the receptor, LDL just floating around in the body, becomes a target for oxidation
-LDL is targeted by macrophages, binds through the scavenger receptor (SR)=> eventually macrophages will die
-cholesterol that accumulates can casue a heart attack
What is reverse cholesterol transport?
-ApoA1 interacts with ABCA1 (transporter) on cells.
-ApoA1 will pick up cholesterol and phospholipids from the cell
-ApoA1 will then begin to make HDL cells, with the help of LCAT, which will make the LDL particles spherical and convert the cholesterol into CE
-HDL can transport cholesterol back into the liver
What is Apo-A1?
-Main ptn of HDL
-Interacts with ABCA1 transporter and activates LCAT (which converts FC to CE)
What is Apo-B100?
-Present on VLDL and LDL
-It contains the region that binds the LDL receptor
What is Apo-B48?
-Present on chylomicrons
-Does NOT contain the region that binds the LDL receptor
What is Apo-E?
-Mediates uptake of remnants to the liver by binding the chylomicron remnants
What can the liver do with FC and CE?
-Store it
-Allow it to be regulatory
-Transform it to VLDL
Which apolipoptns are exchangeable and which are integral?
Integral: Apob48 and ApoB100
Exchangeable: ApoA1 and ApoE
What happens to the mb when LDL is taken up?
When LDL is taken up, cholesterol is also taken up by the cell, gt inc of cholesterol in the ER mb
-SCAP binds cholesterol, won't release SREBP, .: no upregulation of LDLR and HMG-CoA reductase