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CV > 6. Lipoprotein Chemistry > Flashcards

6. Lipoprotein Chemistry Flashcards

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
Q

has apoA-1 and ApoA-2 on surface

A

HDL

26
Q

Characteristics of apolipoprotein

A

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
Q

ApoC II and ApoCIII are on

A

chylomicrons, VLDL, HDL

28
Q

Key features of Exogenous pathway of cholesterol transport

A

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
Q

Key features of Endogenous pathway

A

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
Q

Events in intestine

A
  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
Q

What activates LPL?

A

ApoC II

LPL takes TG —–> FA and glycerol

32
Q

mediates intestinal cholesterol and TG absorption

A

NPC1L1

33
Q

What drug targets NPC1L1

A

Ezetimibe to decrease absorption of TG and cholesterol

34
Q

What transports plant sterols back into intestinal lumen

A

ABCG5/8

body can’t digest plant sterols

35
Q

Mutations in ABCG5/8 is called

A

Sitosterolemia; autosomal Recessive

36
Q

pts that absorb lots of plant sterols–> accumulate in blood and tissues causes tendon and subQ xanthomas and increased risk of premature CHD

A

Sitosterolemia: auto Recessive defect of ABCG5/8

37
Q

What is the main Apo that transports lipids in chylomicrons?

A

ApoB 48

38
Q

Chylomicrons: carry TG and are made from:
Chylomicrons are essential for:
Content of chylomicrons in TG:Chol

A

dietary TG fatty acids + cholesterol from sm. intestine
dietary fat and fat souble vitamins
10:1 (mostly TG)

39
Q

In normolipidemic people, chylomicrons are in plasma for how long after a meal:

A

3-6 hours

should be none 10-12 hours after a fast

40
Q

ApoE is aquired form

A

HDL

41
Q

ApoB 48 is made by:

A

inestinal epithelial cells and is 48% wt of apo-100

42
Q

What is the significance of ApoC-II?

A

activates LPL to allow FFA release for fuel in adipose, heart, skeletal muscle

43
Q

Where is LPL found and what do we need it for

A

bound to capillary endothelium in skeletal, heart, adipose

Key for hydrolysing TG from chylomicrons or VLDL into FFA

44
Q

Process of hydorlysis for LPL

A

TG–>DAG–>MAG

45
Q

What is the end result of LPL hydrolysis

A

get a ‘shrunken’ TG rich particle whre cholesterol phospholipids and apolipoproteins are transfered to HDL

46
Q

HIgh glucose–> insulin release stimulated–> LPL is transcriptionally_______

A

upregulated in adipose

47
Q

In prolongued fasting or diabetic ketoacidosis; LPL activity willl _____

A

fall; prevents storage of Fatty acids

48
Q

Where do chylomicron remnants deposit their cholesterol?

A

Liver; do so after depleated of dietary TG via LPL

Chylomicrons –> liver to dumpo off dietary CHOLESTEROL

49
Q

When chylomicrons get to liver, which apo is degraded?

A

apo-48

50
Q

What Apo is a necessary ligand so chylomicrons can get endocytisized in liver via LDL-receptor or LRP?

A

chylomicrons have ApoE as ligand to get into liver

51
Q

What part of chylomicrons are transfered to HDL?

A

Surface lipds and C proteins

52
Q

What is left over in a chylomicron once it’s been depleated by LPL in caplillaries and in the liver?

A

–rest of chylomicron has ApoB, ApoE, some ApoC and depleated of TG adn enriched in CE

53
Q

in plasma lipid metabolism, this dude key for backup receptor needed for uptake of apoE enriched remnants of chylomicrons adn VLDL

A

LRP:::: LDL receptor related protein

54
Q

What dysfnx do we see in type III hyperlipoproteinemia

A

absence of fnx apoE: so no clearance by LDL receptor and LRP–> get increase TG and cholesterol dense lipoproteins in the plasma.

55
Q

VLDL transports _____ lipids

A

endogenous

56
Q

Where are VLDL made?

A

in liver when TG production is stimulated d/t increase in FFA or increased synthesis of FFA from liver

57
Q

What makes of core of VLDL

where does VLDL go form liver

A

CE’s + TGs (from excess FA or excess carbs) + cholesterol –> to core of VLDL
–> to peripheral tissues

58
Q

What apos are in VLDL

A

ApoC I, ApoC-II, ApoC-III and apoE al made in liver

59
Q

What is the role of Microsomal triglyceride transfer protein?

A

transfers TG to VLDL core

tranfsfers TG to chylomicrons in intestine

60
Q

Pt cant make any ApoB containing lipoporteins (chylomicrons, VLDL or LDL), what the heck?

A

dysfunctional MTP = abetaliporpoteinemia (Vit deficiency, fat in stool, devo delays)

CV (11 decks)

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