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MEH- Aboli > Lipid transport > Flashcards

Lipid transport Flashcards

1
Q

What lipids are important signalling molecules?

A

Diacylglycerols

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2
Q

Plasma concentration range of total cholesterol

A

<5 mmol/L

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3
Q

Plasma concentration range of total lipids

A

4000-8500 mg/L

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4
Q

What polar head group is the most common in phospholipids?

A

Choline- phosphatidylcholine

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5
Q

What phospholipid head group is important in cellular signalling?

A

Inositol- phosphatidylinositol

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6
Q

How is cholesterol obtained?

A

Some from diet but mainly synthesised in liver

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7
Q

What steroid hormones is cholesterol the precursor of (4 things)?

A
  • Cortisol
  • Aldosterone
  • Testosterone
  • Oestrogen
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8
Q

What enzymes are used to esterify cholesterol to make cholesterol esters (2 things)?

A
  • LCAT
  • Acyl~CoA: cholesterol acyltransferase
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9
Q

What do lipoproteins consist of (4 things)?

A
  • Peripheral apolipoproteins
  • Integral apolipoproteins
  • Phospholipid monolayer with small amount of cholesterol
  • Cargo: triacylglycerol, cholesterol esters, fat soluble vitamins
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10
Q

What are the 5 distinct classes of lipoproteins?

A
  • Chylomicron (mainly dietary fat transportation)
  • VLDL
  • IDL (intermediate)
  • LDL (bad cholesterol)
  • HDL (good cholesterol)
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11
Q

Which lipoproteins are main carriers of fat (2 things)?

A
  • Chylomicron
  • VLDL
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12
Q

Which lipoproteins are main carriers of cholesterol esters (3 things)?

A
  • IDL
  • LDL
  • HDL
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13
Q

Apolipoproteins key points (5 things)

A
  • Proteins
  • 6 major classes (A,B,C,D,E & H)
  • Structural role of packaging water insoluble lipid
  • Co-factor for enzymes
  • Ligands for cell surface receptors
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14
Q

Chylomicron metabolism (7 things)

A
  • Loaded in small intestine and apoB-48 added before entering lymphatic system
  • Travel to thoracic duct which empties in left subclavian vein
  • Acquire apoC & apoE once in blood
  • apoC binds lipoprotein lipase on adipocytes & muscle
  • Released fatty acids enter cells depleting chylomicron of content
  • When ~20%, apoC dissociates and chylomicron becomes chylomicron remnant
  • Return to liver: LDL receptor on hepatocytes binds apoE and remnant taken up via receptor-mediated endocytosis
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15
Q

VLDL metabolism (4 things)

A
  • apoB100 added during formation & apoC + apoE added from HDL particles in blood
  • VLDL binds to LPL on muscle endothelium
  • Starts to become depleted of triacylglycerol
  • Used as energy in muscle but stored as fat in adipose
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16
Q

IDL & LDL metabolism (4 things)

A
  • As TAG content of VLDL drops, they dissociate from LPL enzyme complex and return to liver
  • If drops to ~30% it becomes a short-lived IDL particle
  • IDL particles can be taken up by liver or rebind to LPL enzyme to further deplete TAG content
  • When ~10% apoC & apoE lost and becomes LDL (high cholesterol)
17
Q

Function of LDL

A

To transport cholesterol- not efficiently cleared by liver though as don’t have apoC or apoE

18
Q

Clinical relevance of LDL (3 things)

A
  • Half-life much longer so more susceptible to oxidative damage
  • Oxidised LDL taken up by macrophages transforming them into foam cells
  • Can build up and contribute to atherosclerotic plaques
19
Q

LDL entering cells via receptor mediated endocytosis (4 things)

A
  • LDL receptors on cells
  • apoB100 acts as a ligand
  • Receptor/LDL complex taken in by endosomes in endocytosis
  • Fuse with lysosomes for digestion to release cholesterol & fatty acids
20
Q

HDL metabolism- synthesis (3 things)

A
  • Nascent HDL synthesised by liver & intestine
  • Can also bud off from chylomicrons
  • Free apoA-I can also acquire cholesterol & phospholipid to form nascent-like HDL
21
Q

HDL metabolism- maturation (2 things)

A
  • Accumulate phospholipids and cholesterol from cells lining blood vessels
  • Hollow core progressively fills and particle takes on more globular shape
22
Q

HDL metabolism- reverse cholesterol transport (3 things)

A
  • Can remove cholesterol from cholesterol-laden cells and return to liver
  • Reduces likelihood of foam cell formation
  • ABCA1 protein facilitates this
23
Q

HDL metabolism- fate of mature HDL (3 things)

A
  • Mature HDL taken up by liver via specific receptors
  • Cells needing more cholesterol can use scavenger receptor to obtain it from HDL
  • Can also exchange cholesterol esters for TAG with VLDL via action of CETP
24
Q

Hyperlipoproteinaemias key points (3 things)

A
  • Caused by over-production or under-removal
  • Defects in enzymes, receptors & apoproteins
  • 6 main types
25
Q

Clinical signs of hypercholesterolemia (3 things)

A
  • Xanthelasma (yellow patches on eyelids)
  • Tendon xanthoma (nodules on tendon)
  • Corneal arcus (white circle around eye- common in older people but not young)
26
Q

Raised serum LDL to atherosclerosis (6 things)

A
  • Oxidised LDL
  • Macrophage engulfs
  • Foam cell formation and fatty streak
  • Fatty streak evolves into atherosclerotic plaque
  • Grows and encroaches on lumen of artery
  • Ruptures and triggers acute thrombosis
27
Q

Treatment of hyperlipoproteinaemias (5 things)

A
  • First diet change then drugs if no response
  • Reduce cholesterol & saturated fats + increase fibre intake
  • More exercise and less smoking
  • Statins to inhibit HMG~CoA reductase
  • Bile salts sequestrate to force liver to produce more bile acids using cholesterol
28
Q

Ideal ranges of cholesterol

A
  • Non HDL: 4mmol/L or less
  • LDL: 3mmol/L or less
  • HDL: over 1/1.2mmol/L (men:women)
  • Total cholesterol:HDL- above 6 is high risk
  • TG: ideally <2mmol/L in fasted sample

MEH- Aboli (6 decks)

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