10/21 Transport of Lipids Flashcards

1
Q

fxn of fibrates

A

increase LPL expression via PPAR-a so TGs are broken down in the blood to FAs

side effects: gallstones and myalgia

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2
Q

VLDL creation

A

in the liver, TGs are packed around ApoB-100 by MTP

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3
Q

ezetimibe

A

inhibits uptake of cholesterol from gut lumen by enterocytes

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4
Q

what other labs can hypertriglyceridemia fuck up

A

increase in VLDL, increase in LDL, increase in cholesterold deposits in blood vessels

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5
Q

HDL role

A

cholesterol from peripheral tissues to liver, prevents improper accumulatio of cholesterol, gives ApoCII and ApoE to other lipoproteins

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6
Q

IDL role

A

when LPL breaks down VLDL, most FAs go into cells, but remaining clump in blood is now called intermediate density lipoprotein. either go to liver for breakdown or become LDL.

cholesterol rich, has ApoE

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7
Q

LDL role

A

from IDL that has returned to the liver, hepatic lipase removes more TGs, now even denser = LDL, delivers C and CE to tissues with LDL receptors

has least amount of TGs

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8
Q

atherosclerosis

A

deposition of LDL in vessel walls can lead to lesions, foam cells, inflammation, smooth m hyperplasia, fibrosis

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9
Q

ApoB-100

A

contains ligand for LDL receptors on liber, main building block of VLDL in liver

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10
Q

MTP

A

packs VLDL in liver

defect: abetalipoproteinemia (cal deficit, night blindness, spinal and neural defects, acanthocytes, vomiting

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11
Q

LPL

A

releases FAs from VLDL in blood
requires ApoCII

(+) insulin, fibrates

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12
Q

ApoA-1

A

building block for HDL in liver

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13
Q

LCAT

A

picked up by HDL in the blood, allows HDL to pick up C, internalize them, and make them CEs

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14
Q

CETP

A

exchanges TGs (from chylomicrons and VLDLs) for CEs (from HDL)

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