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CV > 6. Lipoprotein Chemistry > Flashcards

6. Lipoprotein Chemistry Flashcards

(60 cards)

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1
Q

storage fats made of 3 FAs and a single glycerol backbone. Most often mixed

A

TGs

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2
Q

are independent risk factor of CV disease and if over 1000 increase risk of pancreatitis

A

Triglycerides

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3
Q

precursor for bile acids and steroids
key for membrane of cells
enriched in lipid rafts in areas key for signal transduciton

A

Cholesterol

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4
Q

How is cholesterol cytoxic?

A

excess: forms chol crystals, triggers apoptotic paths, forms toxic oxysterols, fucks with membrane and promotes atherosclerosis

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5
Q

Key four steps of Cholesterol Synthesis

A
  1. Acetate –> 6C mevalonate
  2. Mevalonate–> 5-C isoprene
  3. 6 isoprenes–> 30-C linear squalen
  4. Squalene cyclizes to make four ringed cholesterol
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6
Q

What enZ takes HMG CoA–> mevalonate

A

HMGCoA reductase

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7
Q

What is the RLS and point of regulation for cholesterol synthesis and target of CV drugs?

A

HMG CoA reductase

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8
Q

Takes AcetylCoA + Acetoacetyl-CoA–> HMG CoA

A

HMG CoA Synthase

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9
Q

Squalene–> cholesterol is significant because

A

where plants and animals diverge

we have cyclase to cyclize squalene to cholesterol

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10
Q

Most cholesterol is made in the ______ then exported as:

A

in liver

exported as bile acids, cholesterol or cholesteryl esters

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11
Q

Whats the role of bile acids

A

emulsifies fats: have taurocholic acid that surrounds fat drops to increase SA for attack by lipases

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12
Q

Adrenal gland makes______ from cholesterol

Gonads make_______ from cholesterol

A

mineral and glucocorticoids

progesterone/androgens/estrogens

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13
Q

Which is more non polar: cholesteryl ester or cholesterol

A

CE!; have FA esterified to oxygen

the FA comes from fatty acyl CoA thus more hydrophobic cholesterol that can’t enter membranes

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14
Q

How are Cholesteryl esters (CE) transported?

A

via lipoproteins to other tissues or stored in liver

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15
Q

What is carried on lipoprotein particles?

A

Cholesterol and lipids

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16
Q

Whats is the surface and interior of lipoproteins?

A

Just surface = apoliproteins made of proteins with a phospholipid monolayer
Inside is loaded with Cholesterol, TGs, CEs

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17
Q

What are ‘cholesterols’ are directly athrogenic?

A

LDL, LPa, IDL, VLDL remnants

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18
Q

Has apo48 on surface (some others) and is largest lipoportein

A

Chylomicron

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19
Q

fnx of chylomicron

A

deliver chol + TG from gut to tissues and liver

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20
Q

What is apo structure of VLDL?

Where is VLDL made?

A

apoB100 and others

made in liver

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21
Q

Fnx of VLDL

A

delivers TG to tissues as fatty acids via LPL

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22
Q

short lived liporotein bteween VLDL and LDL

A

IDL; has apoB100

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23
Q

Has apoB-100 only

A

LDL; stays in circulation much longer then other lilpoproteins

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24
Q

this is homologous between LDL and plasminogen

A

Lp(a)

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25
has apoA-1 and ApoA-2 on surface
HDL
26
Characteristics of apolipoprotein
solubilize lipoprotein in circulation, can change confirmation to adjust to content; can activate or inhibit plasma enZ and have ligands for cell surface receptors
27
ApoC II and ApoCIII are on
chylomicrons, VLDL, HDL
28
Key features of Exogenous pathway of cholesterol transport
Eat fat + bile acids--> chylomicrons take up chylomicrons from intestines (have ApoE, CII and B-48) in capillaries, LPL will release FFA to adipose, tissues and muscle Remnants from LPL transported by B-48 and ApoE to liver
29
Key features of Endogenous pathway
Liver releases VLDL (have ApoE, CII, B100) and go to capillaries where LPL will release FFA to adipose/tissue and muscle IDL is whats left and can to to LDL OR Extrahepatic: release HDL (apoA-! or A-II) --> LCAT to just ApoE and B100--> LDL
30
Events in intestine
1. Biles emulsify fats--> make mixed micells 2. intenstinal lipases degrade TGs 3. FAs and other taken up and converted back to TG 4. TG incorporated with chol and apolipoproteins into chylomicrons 5. Chylomicrons move through circulation 6. LPL activated by ApoC-II In capillary takes TG--> FA and glycerol for use
31
What activates LPL?
ApoC II | LPL takes TG -----> FA and glycerol
32
mediates intestinal cholesterol and TG absorption
NPC1L1
33
What drug targets NPC1L1
Ezetimibe to decrease absorption of TG and cholesterol
34
What transports plant sterols back into intestinal lumen
ABCG5/8 | body can't digest plant sterols
35
Mutations in ABCG5/8 is called
Sitosterolemia; autosomal Recessive
36
pts that absorb lots of plant sterols--> accumulate in blood and tissues causes tendon and subQ xanthomas and increased risk of premature CHD
Sitosterolemia: auto Recessive defect of ABCG5/8
37
What is the main Apo that transports lipids in chylomicrons?
ApoB 48
38
Chylomicrons: carry TG and are made from: Chylomicrons are essential for: Content of chylomicrons in TG:Chol
dietary TG fatty acids + cholesterol from sm. intestine dietary fat and fat souble vitamins 10:1 (mostly TG)
39
In normolipidemic people, chylomicrons are in plasma for how long after a meal:
3-6 hours | should be none 10-12 hours after a fast
40
ApoE is aquired form
HDL
41
ApoB 48 is made by:
inestinal epithelial cells and is 48% wt of apo-100
42
What is the significance of ApoC-II?
activates LPL to allow FFA release for fuel in adipose, heart, skeletal muscle
43
Where is LPL found and what do we need it for
bound to capillary endothelium in skeletal, heart, adipose | Key for hydrolysing TG from chylomicrons or VLDL into FFA
44
Process of hydorlysis for LPL
TG-->DAG-->MAG
45
What is the end result of LPL hydrolysis
get a 'shrunken' TG rich particle whre cholesterol phospholipids and apolipoproteins are transfered to HDL
46
HIgh glucose--> insulin release stimulated--> LPL is transcriptionally_______
upregulated in adipose
47
In prolongued fasting or diabetic ketoacidosis; LPL activity willl _____
fall; prevents storage of Fatty acids
48
Where do chylomicron remnants deposit their cholesterol?
Liver; do so after depleated of dietary TG via LPL | Chylomicrons --> liver to dumpo off dietary CHOLESTEROL
49
When chylomicrons get to liver, which apo is degraded?
apo-48
50
What Apo is a necessary ligand so chylomicrons can get endocytisized in liver via LDL-receptor or LRP?
chylomicrons have ApoE as ligand to get into liver
51
What part of chylomicrons are transfered to HDL?
Surface lipds and C proteins
52
What is left over in a chylomicron once it's been depleated by LPL in caplillaries and in the liver?
--rest of chylomicron has ApoB, ApoE, some ApoC and depleated of TG adn enriched in CE
53
in plasma lipid metabolism, this dude key for backup receptor needed for uptake of apoE enriched remnants of chylomicrons adn VLDL
LRP:::: LDL receptor related protein
54
What dysfnx do we see in type III hyperlipoproteinemia
absence of fnx apoE: so no clearance by LDL receptor and LRP--> get increase TG and cholesterol dense lipoproteins in the plasma.
55
VLDL transports _____ lipids
endogenous
56
Where are VLDL made?
in liver when TG production is stimulated d/t increase in FFA or increased synthesis of FFA from liver
57
What makes of core of VLDL | where does VLDL go form liver
CE's + TGs (from excess FA or excess carbs) + cholesterol --> to core of VLDL --> to peripheral tissues
58
What apos are in VLDL
ApoC I, ApoC-II, ApoC-III and apoE al made in liver
59
What is the role of Microsomal triglyceride transfer protein?
transfers TG to VLDL core | tranfsfers TG to chylomicrons in intestine
60
Pt cant make any ApoB containing lipoporteins (chylomicrons, VLDL or LDL), what the heck?
dysfunctional MTP = abetaliporpoteinemia (Vit deficiency, fat in stool, devo delays)

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