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Cardio 1 > Lipoprotein Metabolism > Flashcards

Lipoprotein Metabolism Flashcards

1
Q

Why do we need lipoproteins

A

They solubilize and move nonpolar liquid through the blood, lymph, and CSF

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2
Q

Major core lipid of each class

A

Triglycerides - VLDL and chylomicrons

Cholesterol- others

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3
Q

Major apolipoproteins of each class

A

Chylo - ApoB48
VLDL - ApoB48
IDL and LDL - ApoB100

HDL - ApoA1

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4
Q

Screen for lipoprotein measutres

A

Totoal C
HDL
TGs

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5
Q

LDL cholesterol

A

LDL=Total-(HDL+Tg/5_

Underestimates if TG over 400 or normal LDL and hypertriglyceridemia

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6
Q

Lipoprotein ultracentrifugation

ApoB ELISA

NMR lipoprotein analysis

A

Direct VLDL-C and LDL-C

Info on Chylo, VLDL and LDL

Data on size and numebr of all

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7
Q

Lipid absorption

A

Emulsification

Hydrolysis of TGs to FA and MG

SOlubilizatioi of FA, MG< FC by bile salts

Transport of FA, MG, and FC into enterocytes and incorporation into lipoprptiens

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8
Q

Peripheral cap endothlium and chylomicrons

A

Will hydrolyze the apolipoprotein into FA (CD26) and leave a remnant

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9
Q

What do you need for hepatic binding and uptake of chylomicron remnants

A

ApoE

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10
Q

LDL synthesis and secretion in the level

A

ApoB100 becomes precursore lipoiprotein via MTP1…this then collects lipid droplets and becomes VLDL

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11
Q

Production and clearance ofVLDL

A

Produced by liver…can become remnant….remnant can become LDL or HDL (via CETP)

LDL or VLDL remnant back to liver

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12
Q

Hepatic binding and uptake of VLDL remnantns

A

Facilitated by ApoB100 or ApoE

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13
Q

Hypertriglyceridemia

A

150-10000

Insulin resistance, CKD< alcohol overuse and pregnancy also cause

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14
Q

How does ApoC3 induce hypertriglyceridemia

A

Inhibits LPL on endothelium so cannot cleave TG into lipoprotein

Disrupts clearance of TLRs by LDL family receptors

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15
Q

Severe hypertriglyceridemia sx

A

Eruptive xanthoma - lipid rich skin lesions
Liemic plasma (over 1000)
Lipemia retinalis - creamy appearance of retinal blood vessels

Hepatosplenomegaly
Pancreatitis

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16
Q

Severe hypertriglyceridemia genetics

A

AUto rec

LPL, APoC2, APOA5, GPIHBP1

17
Q

Production and clearance of LDL

A

VLDL produced, becomes remnant, then LDL…LDL can can back to liver or be stroed in cells as CE

18
Q

Dec LDLR in liver

A

Will increased LDL-C

19
Q

IMpact of dietary fat

A

LDL cholesterol levels

Replace SFA with PUFA

Upregulates LDL and dec VLDL to LDL conversion

20
Q

FH

A

Familai hypercholesterolemia

Auto dom with gene dosage effect

Orange-yellow xanthoma

21
Q

Genetic causes of FH

A

LDLR is most common - reduced LDL receptor expression or function

22
Q

Protective mutations - LDL cholesterol

A

Pro-PCSK9

Mediates the degradation of the LDL receptor

23
Q

HDL functions

A 
anti-ox
Anti-inflam
Cholesterol efflux and reverse trnapsort
ANti-thrombotic
Vasodfilation
24
Q

SR-BI

A

Medaitve selective uptake of cholestryl ester from HDL

25
Q

What dec HDL

A

Insulin resistantce and other hypertriglyceridemic states

26
Q

ApoB48
ApoB100
ApoC2

A

Chlyomicron formation
VLDL formation and clearance of LDL by binding to LDLR
Cofactor for LPL

27
Q

ApoE
ApoC3
ApoA1

A

Ligand for LDL fam receptor that allows effi clearance of triglyceride rich Lipoproteins by liver

inhibitor of triglyceride rich lipoproteins clearance by the liver

HDL formation and cofactor for lecithin (LCAT)

28
Q

MTTP
MPC1L1
LPL

A

Lipidates apoB and is necessary for chylomicron and VLDL formaiton

Mediates uptake of cholestero linto enterycte thus driving absorption

Hydrolyuzes TGs to FA on chylomicrons and VLDL thus driging fatty acid uptake into adipose and muscel

29
Q

LDLR
PCSK9
CETP

A

Critical receptor for clearance of TG rich lipoproteins and LDL

Reduces LDLR levels by binding to and uinducing the lysosomal degradation of the LDLR

Mediate exchange of VLDL triglyceride for HDL cholesterol ester

Cardio 1 (30 decks)

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