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5: MBOD Get Pumped haha > Lipoprotein Metabolism 1 & 2 Khan > Flashcards

Lipoprotein Metabolism 1 & 2 Khan Flashcards

1
Q
  1. What is the purpose of a lipoprotein?
A
  1. Provide a thermodynamically stable particle to transport lipid through bloodstream
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2
Q
  1. What kind of lipoproteins are present in the liver?
A
  1. VLDL,LDL,HDL
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3
Q
  1. What kind of lipoproteins are present in the intestine?
A
  1. CM, small amounts of vldl, hdl
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4
Q
  1. Which lipoprotein is the largest in size?
A
  1. CM
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5
Q
  1. Which lipoprotein transports most of the cholesterol?
A
  1. LDL
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6
Q
  1. What are surface peptides of lipoprotein particles with lipid binding properties?
A
  1. Apolipoproteins
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7
Q
  1. What role do apolipoproteins have?
A
  1. Assembly,secretion, peripheral metabolism and clearance of lipoproteins
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8
Q
  1. What are the functions of ApoB‐100?
A
  1. From liver, essential for VLDL packaging and secretion (contains LDLR domain)
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9
Q
  1. What are the functions of ApoB‐48?
A
  1. Intestinal form, essential for CM packing and secretion, lacks LDLR
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10
Q
  1. What is the function of Apo A‐1?
A
  1. Major apolipoprotein of HDL, co factor for LCAT which esterfies free cholesterol into
    HDL’s
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11
Q
  1. How is the mRNA for Apo‐B edited in making B‐48 instead of B‐100?
A
  1. Single base pair substation, inserts stop codon using APOBEC‐1 complex that has a
    mooring sequence to help precisely insert A for a C
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12
Q
  1. What is the function of Apo A‐IV?
A
  1. May activate LCAT, lots of functions, decreases eating behavior, prevents
    artherosclerosis, packing of lipid into CM
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13
Q
  1. What is the function of Apo C‐II?
A
  1. Activates LPL which hydrolyzes TG in VLDL and CM’s
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14
Q
  1. What is the function of Apo‐E?
A
  1. Ligand for hepatic chylomicron remant receptor and LDL receptor
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15
Q
  1. What activates LPL?
A
  1. Apo CII
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16
Q
  1. What is the function of HL?
A
  1. Remnant lipoprotein uptake, attached to heparin sulfate PG on hepatocytes
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17
Q
  1. What is the function of LCAT?
A
  1. Transfer of fatty acid from lecithin to free cholesterol in HDL
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18
Q
  1. What activates LCAT?
A
  1. Apo A1
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19
Q
  1. What is the function of ABCA1/ABCG1?
A
  1. Mediate phospholipid/cholesterol efflux from cells to lipid poor Apo A1 in reverse
    cholesterol transport
20
Q
  1. What is the rate limiting step of cholesterol synthesis?
A
  1. HMG CoA reductase
21
Q
  1. What is the function of ACAT?
A
  1. Conversion of free cholesterol to cholesterol ester
22
Q
  1. What does LDL receptor bind to?
A
  1. ApB‐100, ApoE and LDL
23
Q
  1. What is the function of LRP?
A
  1. Heptake uptake of remnant CM
24
Q
  1. What is the function of SR‐BI?
A
  1. Hepatic uptake of cholesteryl ester from HDL in reverse cholesterol transport
25
Q
  1. How does HDL take cholesterol back to the liver (enzyme)?
A
  1. Via SRBP1 (scavenger receptor B1)
26
Q
  1. Where are FA re‐esterefied?
A
  1. ER
27
Q
  1. Where are CM’s assembled?
A
  1. ER
28
Q
  1. Where is the final processing of apolipoproteins/lipids for basolateral secretion?
A
  1. Golgi
29
Q
  1. Describe the pathway of FA from exogenous sources
A
  1. Intestinal epithelium –> FABP –> ApoB‐48CM via MTPPCTV –> Golgi –> Secretion
30
Q
  1. What transfers lipid from ER membrane to newly translated apo B ?
A
  1. Microsomal Triglyceride transfer protein
31
Q
  1. What is another function of MTP?
A
  1. Transfer bulk lipid from ER membrane to lumen for further lipoprotein particle
    lipidation
32
Q
  1. Is transfer of CM to Golgi via PCTV microtubule dependent?
A
  1. No
33
Q
  1. Is transfer of CM from golgi to BLM microtubule dependent?
A
  1. Yes
34
Q
  1. Describe Exogenous CM metabolism
A
  1. CM from intestines w/ApoB‐48 –> E and CII attach and activate LPL, CII recycled to
    HDL –> chylomicron remnants into Liver
35
Q
  1. Describe Endogenous CM metabolism
A
  1. ApoB‐100 CM –> LDL to release FA, cholesterol recycled via ABCG1/A1
36
Q
  1. Describe reverse cholesterol transport
A
  1. SRB1 removes cholesterol and stores in hepatocyte –> ABCA1/ApoA1 form pre beta
    HDL which takes up cholesterol from peripheral tissues (ABCA1/G1 fxn) and esterfies
    cholesterol and HDL molecules via LCAT for transfer back to liver
37
Q
  1. What is the role of SREBP?
A
  1. Bound to SCAP which measures concentration of oxytrols (indicator of cholesterol)
    when cholesterol is low SREBP is released and LDLR’s are upregulated, leads to increase
    in cholesterol levels in the cell
38
Q
  1. What levels indicate risk for cholesterol?
A
  1. 5.2mmol/L, 200mg/dL
39
Q
  1. Totalcholesterol=300mg/dL,HDL=100,TG=100,whatisLDL(mg/dL)
A
  1. 180
40
Q
  1. Total cholesterol =300 mg/dL, HDL= 100 , TG=100, what is LDL (mmol/L)
A
  1. 155
41
Q
  1. Do lifestyle changes effect monogenic dyslipidemia’s?
A
  1. Typically not, most require drug therapy, whereas polygenic is opposite
42
Q
  1. What is the defect in familial hypercholesterolemia?

Familial combined
hyperlipidemia?

Familial dysbetalipoproteinemia?

A
  1. LDL receptor,

overproduction ApoB100,

E2/E2 isoform defective remnant binding to
LDL receptor

43
Q
  1. Elevalated levels of Apo (a) and Lp (a) are associated with what?
A
  1. Promoting clot formation on atherosclerotic plaques (LDL bound to ApoA looks like
    kringles)
44
Q
  1. Describe the mechanism of atherosclerosis
A
  1. Damage –> LDL enters through broken epithelium –> LDL is oxidized –> adhesion factors
    expressed & monocytes bind –> Macrophages have scavenger receptor to bind oxidized LDL & internalizes it –> Macrophage becomes overloaded with LDL and is now called foam cell –> cytokines etc. form plaque on endothelial layer & produce metalloproteinases that can break down collagen, platelets bind and initiate thrombus that can cause MI
45
Q
  1. T or F: A stable atherosclerotic plaque has a thin fibrous cap.
A
  1. F

5: MBOD Get Pumped haha (7 decks)

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