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MEH unit > S4) Lipid Transport > Flashcards

S4) Lipid Transport Flashcards

1
Q

Lipids are a structurally diverse group of compounds.

Categorise lipids

A
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2
Q

Lipids are hydrophobic molecules, hence insoluble in water.

How are they transported in light of this?

A

Lipids are transported in blood bound to carriers

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3
Q

How are different types of lipids transported in the blood?

A
  • ~ 2% of lipids (fatty acids) are carried bound to albumin (limited capacity)
  • ~ 98% of lipids are carried as lipoprotein particles consisting of phospholipid, cholesterol, cholesterol esters, proteins & TAG
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4
Q

Describe the structure of a phospholipid molecule

A
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5
Q

Where are phospholipid molecules seen?

A
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6
Q

Describe the formation and function of cholesterol

A
  • Formation: some obtained from diet, but most synthesised in liver
  • Function: essential component of membranes (modulates fluidity)
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7
Q

Cholesterol also acts as a precursor for several molecules.

Identify some

A
  • Precursor of steroid hormones e.g. cortisol, aldosterone, testosterone
  • Precursor of bile acids
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8
Q

How is cholesterol transported?

A

Transported around body as cholesterol ester

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9
Q

Describe the structure of a lipoprotein molecule

A
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10
Q

What are the contents of a lipoprotein molecule?

A
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11
Q

What are the two types of apolipoproteins found on a lipoprotein molecule?

A
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12
Q

There are five distinct classes of lipoproteins named according to density.

Identify them

A
  • Chylomicrons
  • VLDL (very low density lipoproteins)
  • IDL (intermediate density lipoproteins)
  • LDL (low density lipoproteins)
  • HDL (high density lipoproteins)
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13
Q

Illustrate how each type of lipoprotein contains variable content of apolipoprotein, triglyceride, cholesterol and cholesterol ester

A
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14
Q

Lipoprotein density is obtained by flotation ultracentrifugation.

What is the observed relationship between density and diameter?

A

Particle diameter is inversely proportional to density

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15
Q

Rank the different lipoprotein molecules according to their density and diameter

A
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16
Q

What is the relationship between lipoproteins and apolipoproteins?

A

Each class of lipoprotein particle has a particular complement of associated proteins (apolipoproteins)

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17
Q

Which two apolipoproteins are of clinical significance?

A
  • apoB (VLDL, IDL, LDL)
  • apoAI (HDL)
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18
Q

Identify the two roles of apolipoproteins

A
  • Structural: packaging water insoluble lipid
  • Functional: co-factor for enzymes and ligands for cell surface receptors
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19
Q

In 8 steps, outline chylomicron metabolism

A

⇒ In small intestine, apoB-48 added to chylomicrons before entering lymph

⇒ Travel to thoracic duct & empties into left subclavian vein

⇒ Acquire 2 new apoproteins (apoC and apoE) once in blood

⇒ apoC binds lipoprotein lipase on adipocytes and muscle

⇒ Released FA enter cells depleting fat content in chylomicron

⇒ Chylomicron remnants return to liver

⇒ LDL receptor on hepatocytes binds apoE, chylomicron remnant taken up by receptor mediated endocytosis

⇒ Lysosomes release remaining contents for metabolic use

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20
Q

What are chylomicron remnants?

A

Chylomicron remnants are molecules formed when triglyceride content is reduced to ~20% and apoC dissociates

21
Q

What is lipoprotein lipase and where is it found?

A
  • LPL is an enzyme that hydrolyses TAG in lipoproteins and requires ApoC-II as cofactor
  • It is found attached to surface of endothelial cells in capillaries
22
Q

In 5 steps, outline VLDL metabolism

A

⇒ In liver, apoB100 added during formation

⇒ apoC and apoE added from HDL particles in blood

⇒ VLDL binds to LPL on endothelial cells in muscle and adipose

⇒ TAG content depletes

⇒ Released FA used for energy production (muscle) / re-synthesis of TAG and fat storage (adipose)

23
Q

In four steps, explain how IDL and LDL are formed from VLDL

A

⇒ VLDL particles dissociate from LPL as TAG content depletes and return to liver

⇒ IDL particle is formed if VLDL content depletes to ~30% (short lived)

⇒ IDL particles can return to liver / rebind to LPL enzyme to further deplete TAG content

⇒ LDL particle is formed if depletion to ~ 10% as IDL loses apoC & apoE

24
Q

Illustrate the relationship between VLDL, IDL and LDL metabolism

A
25
Q

Describe the structure and function of the LDL particle

A
  • Structure: do not have apoC or apoE, hence aren’t efficiently cleared by liver (liver LDL-Receptor has a high affinity for apoE)
  • Function: provide cholesterol from liver to peripheral tissues (peripheral cells LDL receptor takes up LDL via receptor mediated endocytosis)
26
Q

The IDL particle is short lived in comparison to the LDL particle.

What is the clinical relevance of this?

A
  • Half life of LDL in blood is much longer than VLDL or IDL making LDL more susceptible to oxidative damage
  • Oxidised LDL taken up by macrophages that can transform to foam cells and contribute to formation of atherosclerotic plaques
27
Q

In four steps, describe how LDL enters peripheral cells by receptor mediated endocytosis

A

⇒ Cells requiring cholesterol express LDL receptors on plasma membrane

⇒ apoB-100 on LDL acts as a ligand for these receptors

⇒ Receptor/LDL complex taken into cell by endocytosis into endosomes

⇒ Fuse with lysosomes for digestion to release cholesterol and fatty acids

28
Q

What controls the receptor-mediated endocytosis of LDL in peripheral cells?

A

LDL receptor expression controlled by cholesterol concentration in cell

29
Q

Describe the three possible pathways for the synthesis of HDL

A
  • Synthesised by liver and intestine (low TAG levels)
  • Bud off from chylomicrons and VLDL as they are digested by LPL
  • Free apoA-I acquires cholesterol and phospholipid from other lipoproteins and cell membranes
30
Q

How do HDL particles mature?

A
  • Nascent HDL accumulates phospholipids and cholesterol from cells lining blood vessels
  • Hollow core progressively fills and particle takes on more globular shape
31
Q

Explain the role of HDL in reverse cholesterol transport

A
  • HDL remove cholesterol from cholesterol-laden cells and return it to liver
  • ABCA1 protein within cell facilitates transfer of cholesterol to HDL
  • Cholesterol then converted to cholesterol ester by LCAT
32
Q

What is the clinical relevance of reverse cholesterol transport?

A

Reduces likelihood of foam cell and atherosclerotic plaque formation in blood vessels

33
Q

What is the fate of mature HDL particles?

A

Mature HDL taken up by liver via specific receptors and degraded by lysosomes

34
Q

Describe the role of HDL in cholesterol transfer

A
  • Cells requiring additional cholesterol, e.g. for steroid hormone synthesis, can also utilise scavenger receptor (SR-B1) to obtain cholesterol from HDL
  • HDL can also exchange cholesterol ester for TAG with VLDL via action of cholesterol exchange transfer protein (CETP)
35
Q

Illustrate a summary of HDL metabolism in terms of the following:

  • Formation
  • Maturation
  • Reverse cholesterol transport
  • Cholesterol transfer
  • Breakdown
A
36
Q

What are hyperlipoproteinaemias?

A
  • Hyperlipoproteinaemias are conditions causing a raised plasma level of 1/more lipoprotein classes as a result of over-production or under-removal
  • This occurs due to defects in enzymes, receptors or apolipoproteins
37
Q

What is hypercholesterolaemia?

A
  • Hypercholesterolaemia is a condition where there is a high level of cholesterol in blood
  • It presents with cholesterol deposits in various areas of body
38
Q

Identify and describe the three clinical signs of hypercholesterolaemia

A
  • Xanthelasma – yellow patches on eyelids
  • Tendon xanthoma – nodules on tendon
  • Corneal arcus – obvious white circle around eye (common in older people)
39
Q

Raised serum LDL is associated with atherosclerosis.

Outline the pathway in which oxidised LDL leads to angina, myocardial infarction or stroke due to atherosclerosis

A
40
Q

Illustrate the different stages between plaque formation and plaque rupture

A
41
Q

The first approach of treating hyperlipoproteinaemias is conservative.

Describe the conservative treatment of this condition

A
  • Diet – reduce cholesterol and saturated lipids in diet and increase fibre intake
  • Lifestyle – increase exercise and stop smoking to reduce cardiovascular risk
42
Q

The first approach of treating hyperlipoproteinaemias is specific.

Describe the pharmacological treatment of this condition

A
  • Statins – reduce cholesterol synthesis by inhibiting HMG-CoA reductase
  • Bile salt sequestrants – bind bile salts in GI tract and forces liver to produce more bile acids using more cholesterol
43
Q

Describe the method of action of statin drugs in the pharmacological treatment of hyperlipoproteinaemias

A
44
Q

Identify and describe the 6 different cholesterol tests available

A
  • Total Cholesterol – ideally 5 mmol/L or less
  • Non HDL-Cholesterol – ideally 4mmol/L or less
  • LDL-Cholesterol – ideally 3 mmol/L or less
  • HDL-Cholesterol – ideally over 1-1.2mmol/L (men&women)
  • Total cholesterol:HDL-C ratio – ratio > 6 considered high risk
  • Triglyceride – ideally < 2mmol/L in fasted sample
45
Q

if a person hasnt eaten in over 15 hours will they have chylomirons present

A

no, as they carry dietry fats

46
Q

is cholesterol synthesised in the body

A

yes LDLs synthesise them

47
Q

whats an angina

A

reduced blood flow to the heart

48
Q
A

MEH unit (6 decks)

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