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FoundSci Unit 4 > Lipid Transport > Flashcards

Lipid Transport Flashcards

1
Q

What is the structure of a lipoprotein?

A

Hydrophobic core with triglycerides, cholesteryl esters

Surrounded with single-layer membrane with charges on outside that interact with aq surroundings

Proteins embedded in surface membrane

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2
Q

What proteins are embedded in surface membrane of lipoproteins?

A

Apo-proteins - for structural support and for interactions with receptors and catalytic proteins

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3
Q

Describe the transport of lipids with albumin

A

Free fatty acids are released from adipose tissue followed by wave of ketones

Neither require special transport and just bind to hydrophobic pockets on albumin while ketone bodies dissolve readily in serum

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4
Q

Describe the transport of lipids with lipoproteins

A

Lipid transport from enterocytes and liver require lipoproteins.

Triglycerides/cholesterol are released by enterocytes and liver and are loaded into lipoproteins through hydrophobic interactions. Amphipathic FA are converted to hydrophobic TG, cholesterol esterified to cholesteryl esters.

TG and CE form the hydrophobic core of lipoproteins and are shielded from hydrophilic environment

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5
Q

How are lipids unloaded from the lipoprotein?

A

Hydrolysis of TG by lipoprotein lipase releases FA

Hydrolysis of Cholestryl esters by cholesterol esterase releases cholesterol

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6
Q

What are the three routes of lipoprotein lipid traffic?

A
  1. Distribution of dietary lipids via chylomicron
  2. Distribution of lipids made by the liver: VLDL -> IDL -> LDL
  3. Transport of cholesterol to the liver for excretion: HDL
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7
Q

What creates serum turbidity after a meal?

A

Chylomicrons. They are the largest lipoproteins

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8
Q

Describe the distribution of dietary lipids

A

Lipids absorbed by the diet are packed into chylomicrons by enterocytes.

Chylomicrons deliver TG to muscles for consumptions and adipose tissue for storage

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9
Q

Describe the distribution of lipids made in the liver

A

Liver synthesizes lipids in the fed state and packs them into very low density lipoproteins (VLDL)

VLDLs distribute lipids to muscles and adipose tissue and get smaller and denser, turning into intermediate density lipoproteins (IDL) and low density lipoproteins (LDL)

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10
Q

When are VLDLs made?

A

Synthesized during fasting state to be used in fed state

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11
Q

Describe the transport of cholesterol to the liver for excretion

A

Liver synthesizes empty high density lipoproteins (HDL) that absorb cholesterol from peripheral tissues and transport it back to the liver for excretion

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12
Q

What is the triglyceride and cholesterol content of lipoproteins?

A

Chylomicrons - mostly TG (99%)

VLDL - contain TG and some cholesterol (92% TG and 8% chol)

IDL - 85% TG, 15% chol

LDL - 80% TG, 20% chol

HDL - mostly cholesterol, 50% TG, 50% chol

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13
Q

What occurs with defects in lipoprotein synthesis?

A

Hypolipidemia

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14
Q

What occurs with defects in lipoprotein unloading?

A

Hyperlipidemia

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15
Q

What are characteristics of hyperlipidemia?

A

Elevated TG and/or cholesterol

Risk for cardiovascular disease

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16
Q

What is primary dyslipidemia?

A

Abnormal concentration of serum lipids. Congenital disorders caused by mutations in lipoprotein metabolism.

Most frequent cause of dyslipidemia in children and often dominant mode of inheritance where a parent is affected

17
Q

What are apoproteins?

A

Proteins in the outer membrane of lipoproteins that support structure and regulate function of the lipoprotein

18
Q

What are the apoproteins for structural support?

A

ApoB48 - in Chylomicrons
ApoB100 - in VLDL, IDL, LDL
ApoA - in HDL

Interact with receptors on the surface of target cells

ApoB100 and ApoB48 are encoded by same gene - variation created by RNA editing

19
Q

What apoprotein regulates fatty acid release from lipoproteins?

A

ApoC-II

Activates lipoprotein lipase on endothelial cells

20
Q

What apoprotein regulates cholesterol entry into lipoproteins?

A

ApoA

Activates Lecithin-Cholesterol Acyltransferase (LCAT) for esterification of cholesterol

21
Q

What apoprotein helps with interaction with lipoprotein receptors?

A

ApoE

A ligand for LDL and scavenger clearance

22
Q

Describe chylomicrons, their apoproteins, and their development

A

Synthesized in enterocytes and transport lipids from diet. They get smaller as they lose lipids and turn into chylomicron remnants

Apoproteins - ApoB48, ApoC-II, and ApoE

23
Q

Describe VLDL, their apoproteins, and their development

A

Synthesized in liver and transports fat and cholesterol from metabolic overflow. Get smaller and heavier as they lose fat and pick up cholesterol, converting to IDL and LDL

Lose ApoCII and then ApoE during transition

Apoproteins - ApoB-100. ApoC-II, ApoE

24
Q

Describe HDL, their apoproteins, and their development

A

Synthesized in liver. Transports cholesterol from body back to liver and get bigger and heavier as they pick up cholesterol. Distribute ApoE and ApoC-II

Apoproteins - ApoA, ApoC-II, ApoE

25
Q

Describe Lipoprotein A, their apoproteins, and their development

A

Function is unclear but is associated with cardiovascular risk

Apoproteins - ApoA-S-S-ApoB100

26
Q

Describe the maturation of chylomicrons

A

Chylomicrons transport lipids from enterocytes around body and begin as non-functional particles filled with TG from the diet

Structural support provided by ApoB-48

After release from enterocytes, chylomicrons obtain ApoC-II and ApoE from HDL

Chylomicrons shrink as they lose lipids (lipoprotein lipase action) and turn to remnants

Chylomicron remnants bind to liver receptors through ApoE interactions and are removed via endocytosis

27
Q

What has to happen to TG before they can enter enterocytes?

A

TG has to be hydrolyzed by pancreatic lipase

28
Q

Describe the maturation of VLDL

A

Liver produces VLDL for fat distribution. Made during fasting and used in fed state

VLDL begins as non-functional particle filled with lipids and cholesterol with structural support provided by ApoB-100

VLDL pick up ApoC-II and ApoE from HDL

Lose TG through lipoprotein lipase and gain cholesterol by transfer with HDL

Transitions to IDL as it loses ApoC-II along with most of its TGs. Becomes LDL as IDL accumulates cholesteryl esters and lose ApoE

LDL binds to LDL receptors to clear contents into cholesterol requiring cells

29
Q

What occurs if LDL accumulates?

A

Surplus LDL either due to overproduction or insufficient clearance, get oxidized and taken up via scavenger receptors which leads to plaque formation in blood vessels

30
Q

Describe maturation of HDLs

A

HDLs begin in liver as empty particles assembled with ApoA scaffold

Deliver ApoC-II and ApoE to maturing chylomicrons and VLDL. Extract cholesterol from membrane and move to liver for excretion

Cholesterol extraction from plasma membranes through ABCA1 and transfer to surface of HD: with lipoprotein collides with membrane

HDL exchanges cholesteryl esters with LDL through CETP

Esterification of cholesterol through LCAT moves cholesterol into HDL for transport to liver where it is converted to bile salt and excreted in feces through bile duct

31
Q

What is secondary dyslipidemia?

A

Consequences of other metabolic disorders and disturbances

Most frequent cause of dyslipidemia in adults

Often caused by poor diet, diabetes, alcohol use

32
Q

Fredrickson Phenotypes

A

Classify dyslipidemia. Incudes 5 classes and allows us to identify the defective component based on observed elevation of serum cholesterol and TG

Elevated lipid fraction clues to lipoprotein

33
Q

How does a patient with Fredrickson IIa present?

A

High LDL

High cholesterol

Family history of hypercholesterlemia

Physical examination shows fatty deposits on Achilles tendons and knuckles

Labs shows elevated cholesterol and normal TG

34
Q

What are possible reasons LDL is elevated in Fredrickson IIa?

A

LDL no binding to receptor - Familial hypercholesteremia (FH), most common primary dyslipidemia

ApoB-100 defective - Familial defective ApoB100 (FDB), 2nd most common. Phenocopy of FH - diagnosis is by detecting of mutation

35
Q

Why does diabetes result in hyperlipidemia?

A

Metabolism permanently in fasting state so adipose tissue constantly releases FAs and so there are too many FAs in circulation

Liver takes up excess FAs and makes TG, assembles VLDL.

Diabetic dyslipidemia characterized by high serum TG

FoundSci Unit 4 (11 decks)

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