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MEH > Lipid transport > Flashcards

Lipid transport Flashcards

1
Q

• Describe how lipids are transported in the blood. (lipolysis)

A
  • TAG in adipose catalysed by hormone sensitive lipase
    • glycerol
      • travels to liver
      • utilised as carbon store for gluconeogenesis
    • fatty acids
      • travels complexed with albumin to muscle & other tissues for β-oxidation
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2
Q

Regulation of lipolysis

A
  • glucagon & adrenaline
    • phosphorylation
    • activation of HSL (hormone sensitive lipase)
  • insulin
    • de-phosphorylation
    • inhibition of HSL
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3
Q

Plasma cholesterol concentration ranges

A

< 5mmol/L

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4
Q

Phospholipid structure

A
  • phosphatidylcholine
    • choline head bonded to glycerol with phosphate group
  • phosphatidylinositol (minor)
    • inositol head bonded to glycerol with phosphate group
      • role in cellular signalling
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5
Q

What is the difference between a liposome & micelle

A
  • liposome
    - bilayer
    - hydrophilic
    • micelle
      • monolayer
      • hydrophobic
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6
Q

Where is cholesterol obtained from

A
  • mostly synthesised in liver
  • some obtained from diet
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7
Q

Uses of cholesterol

A
  • membrane component
    • modulates fluidity
  • precursor of steroid hormones
    • cortisol
    • aldosterone
    • testosterone
    • oestrogen
  • precursor of bile acid
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8
Q

How is cholesterol transported around the body

A

as cholesterol esters

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9
Q

Lipoprotein makeup

A
  • peripheral apolipoproteins
  • integral apolipoprotein
  • phospholipid monolayer with small amount of cholesterol
  • cargo
    • TAG
    • cholesterol ester (c linked to fa)
    • fat soluble vitamins
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10
Q

Peripheral apolipoprotein examples

A
  • apoC
  • ApoE
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11
Q

Integral apolipoprotein

A
  • apoA
  • ApoB
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12
Q

Classes of lipoprotein

A
  • chylomicrons
    • transport dietary fat
  • VLDL (very low density lipoprotein)
    • transports TAG made in the liver to other tissues
  • IDL (intermediate density lipoprotein)
    • short-lived intermediary produced when VLDL content is depleted to ~ 30%
  • LDL
    • produced when IDL contents depleted to ~ 10%
  • HDL
    • transport excess cholesterol from cells to liver
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13
Q

Main carriers of fat

A
  • chylomicron
  • VLDL
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14
Q

Main carriers of cholesterol esters

A
  • IDL
  • LDL
  • HDL
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15
Q

Function of apolipoprotein

A
  • structural
    • packaging water insoluble lipid
  • functional
    • co-factor for enzymes
    • ligands for cell surface receptor
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16
Q

Apoliproteins

A
  • 6 major classes (A, B, C, D, E & H)
  • apoB (VLDL, IDL, LDL) and apoAI (HDL) important
  • either integral or peripheral
17
Q

Describe chylomicron metabolism.

A
  1. loaded into small intestine & apoB-48 added before entering lymphatic system
  2. travel to thoracic duct
    - empties to left subclavian vein
    - acquires apoC and apoE once in blood
  3. apoC binds to lipoprotein lipase (LPL) on adipocytes & muscle
    - fatty acids enter cells, depleting chylomicron’s fat content
  4. when TAG reduced to ~ 20%, apoC dissociates
    - chylomicron becomes chylomicron remnant
  5. remnant returns to liver
    - LDL receptor on hepatocytes bind to apoE
    - remnant taken up by receptor mediated endocytosis
  6. lysosomes release remaining contents for use in metabolism
18
Q

Describe VLDL metabolism.

A
  1. apoB100 added during formation in liver
    • apoC and apoE added from HDL in blood
  2. VLDL binds to LPL on endothelial cells in muscle & adipose
    • TAG depletes
  3. In muscle: released fatty acids taken up & used in energy production
  4. In adipose: fatty acids used for re-synthesis of TAG and stored as fat
19
Q

Lipoprotein lipase (LDL)

A
  • hydrolyses TAG in lipoproteins
  • requires ApoC-II as co-factor
  • attached to surface of endothelial cell in capillaries
20
Q

Describe the features of LDL.

A
  • lost apoC & apoE
    • not efficiently cleared by liver
      • liver LDL-receptor has high affinity for apoE
  • high cholesterol content
    • transports cholesterol from liver to peripheral tissue
      • tissues express LDL receptor
        • take up LDL via receptor mediated endocytosis
21
Q

Clinical relevance of LDL

A
  • half life in blood is longer than VLDL or IDLL
    • more susceptible to oxidative damage
  • oxidised LDL taken up by macrophages → foam cells
    • contribute to atherosclerotic plaque formation
22
Q

Describe the process by which LDL is uptaken by receptor mediated endocytosis

A
  1. LDL receptor expressed on membrane
    • apoB-100 on LDL acts as ligand for receptors
    • expression controlled by cholesterol concentration in cell
  2. LDL complex taken in by endocytosis into endosomes
  3. Endosome fuse with lysosome for digestion to release cholesterol and fatty acids
23
Q

HDL synthesis

A
  • by liver + intestine
  • can also bud off chylomicrons & VLDL during digestion by LPL
  • free apoAI can acquire cholesterol + phospholipids from other lipoprotein & cell membrane to form nascent-like HDL
24
Q

Maturation of HDL

A
  • nascent HDL accumulate phospholipids & cholesterol from endothelial cells
    • doesn’t require enzyme activity
25
Q

Describe the role of reverse cholesterol transport in preventing atherosclerosis.

A
  • HDL can remove cholesterol from cholesterol-laden cells & return it to liver
    • reduces likelihood of foam cells & atherosclerotic plaque formation
      • facilitated by ABCA1 protein
        • cholesterol converted to cholesterol ester by LCAT
26
Q

Describe the fate of mature HDL

A
  • taken up by liver via specific receptors
  • cells requiring additional cholesterol utilise scavenger receptor (SR-B1)
    • obtains cholesterol from HDL
  • HDL can exchange cholesterol esters for TAG with VLDL
    • via action of cholesterol exchange transfer proteins (CETP)
27
Q

What are hyperlipoproteinaemias

A
  • raised plasma levels of ≥ 1 lipoprotein classes
    • caused by over-production or under-removal
28
Q

Types of hyperlipoproteinaemias

A
  • I
    • Chylomicrons in fasting plasma.
    • No link with coronary artery disease.
    • Caused by defective lipoprotein lipase
  • IIa
    • Associated with severe coronary artery disease
    • Caused by defective LDL receptor
  • IIb
    • Associated with coronary artery disease.
    • Defect unknown.
  • III
    • Raised IDL and chylomicron remnants.
    • Associated with coronary artery disease.
    • Rare
    • Caused by defective apoE
  • IV
    • Associated with coronary artery disease.
    • Defect unknown.
  • V
    • Raised chylomicrons and VLDL in fasting plasma.
    • Associated with coronary artery disease.
    • Cause unknown
29
Q

Clinical signs of hypercholesterolaemia

A
  • high blood cholesterol
  • cholesterol deposition in various areas of body
    • xanthelasma
      • yellow patches on eye lids
    • tendon xanthoma
      • nodules on tendon
    • corneal arcus
      • white/blue circle around eye
      • common in older people, but indicative of disease in younger people
30
Q

Describe how raised serum LDL is associated with Atherosclerosis.

A
  1. oxidised LDL recognised by macrophages
  2. foam cells (lipid laden macrophages) accumulate in intima of blood vessel walls
    - forms fatty streak
  3. fatty streak evolves into atherosclerotic plaque
  4. grows & encroaches on artery lumen
    • angina
  5. rupture
    • triggers acute thrombosis (clot) by activating platelets & clotting cascade
      > stroke
      => myocardial infarction
31
Q

• Explain the first response in how hyperlipoproteinaemias may be treated.

A
  • diet
    - reduce cholesterol & saturated lipids
    - increase fibre intake
  • lifestyle
    - increase exercise
    - stop smoking to reduce CVD risk
32
Q

. Explain how hyperlipoproteinaemias may be treated if initially treatment is unresponsive

A
  • statins
    - reduce cholesterol synthesis
    - inhibiting HMG-CoA reductase
  • bile salt sequenstrants
    - bind bile salts in GI tract
    - forces liver to produce more bile acids using more cholesterol

MEH (6 decks)

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