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Physiology 3003 > Lecture 14--plasma lipoproteins > Flashcards

Lecture 14--plasma lipoproteins Flashcards

1
Q

3 classes of lipids…

A

(1) Cholesterol(Chol)
(2) Triglycerides(TGs)
(3) Phospholipids (PLs)

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2
Q

Functions of cholesterol

A

(1) structural role

2) Precursor (bile salts, steroid hormones, vit D

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3
Q

Functions of TGs

A

(1) Energy transport/storage
(2) Thermoregulatory (insulation)
(3) Protection of organs

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4
Q

Functions of Phospholipids

A

(1) Membranes
(2) Lipid transport
(3) Nerves
(4) Cell signalling (surface coating of lipoproteins)

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5
Q 
Normal plasma [cholesterol]
LDL chol: \_\_\_
HDL chol: \_\_\_
LDL/HDL ratio: \_\_\_
Total chol: \_\_\_
A

LDL chol: 1 mmol/L

LDL/HDL ratio:

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6
Q

(Normal plasma concentration)

LDL chol: ____mmol/L

A
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7
Q

(Normal plasma concentration)

HDL chol: ____mmol/L

A

> 1 mmol/L

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8
Q

(Normal plasma concentration)

Total chol: ____mmol/L

A
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9
Q

(Normal plasma concentration)

LDL/HDL ratio: ____

A
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10
Q

(Normal plasma concentration)

Triglycerides: ____mmol/L

A
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11
Q

Forms of cholesterol

A

(1) FREE cholesterol

2) Cholesterol esters (storage form) (chol + FA

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12
Q

What’s the composition of lipoproteins (LPs)

A

Central core: TGs & Chol esters

Outer surface coat: Phospholipids, apoproteins, free cholesterol (structural function)

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13
Q

What are LIPOPROTEINS

A

Transport lipids from site of absorption/synthesis to peripheral tissues

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14
Q

what are the 6 classes of lipoproteins

A

(1) Chylomicrons (CM)
(2) CM remnants
(3) VLDL (v. low density)
(4) IDL (Intermediate density)
(5) LDL (low density)
(6) HDL (high density)

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15
Q

What are the main apoproteins found on each class of lipoprotein?

A

**CM–> ApoB-48

  • *VLDL–> ApoB-100
  • *LDL–> ApoB-100 (only apoprotein on LDL)

**ApoCII –> on ALL BUT LDL (i.e. ApoCII–>CM/VLDL/HDL/IDL)

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16
Q

Which LPs have the most TG %?

A

CM and VLDL
CM=90%
VLDL =~60%

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17
Q

In fasted state the dominant TG store is contained in which LP? why?

A

In fasted state VLDL = predominant TG store

Because the short 1/2 life of CM (5-30 minutes) means it is not present in the blood of a fasted individual.

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18
Q

Which LPs have the >best esterified cholesterol content?

A

LDL = 60% esterified cholesterol

19
Q

Why does the density of lipoproteins shift from lowest in CM–>CMremnant–>VLDL–>IDL–>LDL (highest in LDL)?

A

To do with change in composition of LP.
The outer surface coating is made of higher density components than the TG/chol ester core so when the TGs are hydrolysed(and removed from the LP) the outer surface coating makes up a higher fraction of the LP and therefore the density increases.

20
Q

Order the LP classes in order of density (1=most dense, 5=least dense)

A
  1. HDL
  2. LDL
  3. IDL
  4. VLDL
  5. CM
21
Q

Order the LP classes by diameter (1=largest diameter, 5=smallest)

A
  1. CM
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
22
Q

Differentiate CM & VLDL formation (synthesis & secretion)

A

**CM–> synthesised in enterocytes, released into the lymphatic circulation (as too large to diffuse directly into blood)

**VLDL–> synthesised in liver, released directly into circulation

23
Q

What’s bad cholesterol? Why?

A

LDL = bad cholesterol

1) Oxidised readily
2) Taken up by macrophages in arterial walls
3) => Accumulate cholesterol esters = formation of foam cells
4) Atherosclerosis (=>coronary heart disease)

24
Q

A ___% increase in [LDL] –> ____% ___ in CHD risk

A

10% increase in [LDL]

–> 20% increase in CHD risk

25
Q

What is the 1/2 life of a chylomicron?

A

5-30 minutes

26
Q

What is the 1/2 life of VLDL?

A

12 hours

27
Q

What is the 1/2 life of LDL?

A

1-3 days

28
Q

What is the 1/2 life of HDL?

A

5-6 days

29
Q

What apoprotein is expressed on chylomicrons?

A

Apo-B48

30
Q

What is the function of apoproteins

A

(1) MAINTENANCE of LP STRUCTURE (structure/strength)
(2) Regulate LP METABOLISM (cell uptake/metabolism depends on the type of apoprotein)
(3) COFACTOR for enzymes of lipid metabolism

31
Q

On what lipoproteins is Apo-B100 expressed and what is its function?

A

Expressed on VLDL & LDL

is a LIGAND FOR LDL RECEPTORS

32
Q

On what LP is Apo-B48 expressed?

A

Expressed on CM & CM remnants

-receptor binding domain is absent (truncated/missing)

33
Q

On what LP is Apo-CII expressed and what is its function?

A

Expressed on HDL/CM/VLDL/IDL (all but LDL)

Essential cofactor required for hydrolysis of lipoproteins by lipoprotein lipase (interacts with lipoprotein lipase in capillary beds leading to TG hydrolysis)

34
Q

Outline CM formation

A
  1. (Intestinal lumen) Fat emulsified, MICELLES –> absorbed to enterocytes
  2. (ER) FORMATION OF LIPOPROTEINS
    ==>Involves enzymes …ACAT (esterifies cholesterol)
    ==>MTP (microsomal transfer protein, essential for CM formation in enterocytes…packages together the CM)
  3. Released into the LYMPHATIC CIRCULATION
35
Q

What is the function of ACAT

A

Esterifies cholesterol (involved in formation of Chylomicrons)

36
Q

What is the function of MTP

A

Microsomal transfer protein
Essential for CM formation in enterocytes
Packages Chylomicrons

37
Q

What is the EXOGENOUS PATHWAY for lipid metabolism

A

Pathway involving CHYLOMICRONS

(1) Absorbed (Micelles)
(2) Chylomicrons
(3) Released to lymphatics
(4) TGs (in CM) are hydrolysed as they pass through capillary beds & Free FAs are released (Either for energy or storage as lipid droplets in adipocytes)
(5) Left with the CHYLOMICRON REMNANT which is TAKEN UP BY THE LIVER & removed from the circulation

38
Q

What is the ENDOGENOUS PATHWAY for lipid metabolism?

A

(1) Liver => VLDL (released to circulation)
(2) VLDL => IDL + FFA (hydrolysis of TGs when pass over capillaries)
(3) IDL => 1/2 removed from circulation at liver, other 1/2 is metabolised again (IDL=> LDL + FFA)
(4) LDL => Taken up by peripheral tissues

(can easily be oxidised and taken up by macrophages leading to formation of foam cells (=atherosclerosis = CHD)

39
Q

What’s REVERSE CHOLESTEROL TRANSPORT?

A

HDL–>circulation–>removes lipids/chol from peripheral tissue/macrophages/foam cells –>returns them to the liver to be recycled/disposed of

40
Q

What is the role of LIPOPROTEIN LIPASE in lipid metabolism?

A
  • -Present in ADIPOSE TISSUE, MAMMARY GLAND, HEART, MUSCLE
  • ApoCII = essential cofactor (apoprotein on all LPs except LDL)
  • hydrolyses TG as pass over capillary beds in Lipoproteins
41
Q

LDL receptor pathway

A

Delivery of cholesterol from LDL –> Peripheral tissues

LDL receptors
ApoB100 ligands
Binds 
Particle internalised 
Lysosome breaks down LP particle
Receptor = recycled
42
Q

What are the consequences of increasing [chol] in peripheral tissues?

A

(1) REDUCES Cholesterol SYNTHESIS (reduces expression of HMG-CoA REDUCTASE)
(2) INCREASES STORAGE of cholesterol esters in cells (increases synthesis of ACAT (esterifies free cholesterol with FAs)
(3) REDUCES LDL RECEPTOR expression (=reduces LDL uptake)

43
Q

ACAT

A

Esterifies free cholesterol with FA for storage

44
Q

What are the pathways for lipid metabolism?

A

(1) ENDOGENOUS (VLDL-Liver)
(2) EXOGENOUS (CM-Intestine)
(3) REVERSE CHOL TRANSPORT (HDL-Liver)

Physiology 3003 (15 decks)

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