Atherosclerosis 2 Flashcards

1
Q

Does VLDL and remnant particles contain much TAG?

A

They are TAG-rich

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2
Q

What is the Fuel Transport Pathway ?

A
  • Chylomicrons transport TAG to periphery cells, remnants metabolised in liver
  • VLDLs transport fuel from liver to peripheral tissues & remnants return to liver
  • Part of the VLDL remnants & IDL are converted into LDL which enters the overflow
    pathway
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3
Q

What is the Overflow pathway ?

A
  • LDLs travel in blood from liver to the peripheral tissues and back to the liver
  • On their way back they may enter the arterial wall
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4
Q

What can remove TAGs from TAG-rich lipoprotein particles ?

A
  • Hydrolases
  • Lipoprotein lipase (LPL)
  • Hepatic triglyceride lipase
    (HTGL)
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5
Q

What does the LPL do ?

A
  • Digests TAGs in chylomicrons and VLDLs and releases FA & glycerol
    for cell metabolism or storage
  • Also, bind to heparan sulfate proteoglycans on vascular endothelial cells
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6
Q

What is HTGL associated with ?

A

HTGL is associated with liver plasma membranes and acts on particles already digested by LPL

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7
Q

What can humans not metabolise in terms of the structure of the cholesterol?

A

Humans cannot metabolise the cholesterol ring system

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8
Q

What is involved in the reverse cholesterol transport ?

A
  1. CERP (cholesterol efflux regulatory protein)
    - plays major role in cholesterol efflux
  2. LCAT (lecithin:cholesterol acyl transferase)
    - esterifies cholesterol
  3. CETP (cholesterol ester transfer protein)
    - a plasma protein
    - transfers part of its cholesteryl esters to TAG
    rich lipoproteins
    - Binds to scavenger in liver after increasing in size
    - Results in transfer of cholesterol to the cell
    membrane, which is then excreted as free sterol
    or as bile acids
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9
Q

Why are Apolipoproteins important for lipoprotein transport ?

A
  • Solubilise the non-polar lipids in the circulation

- Interact with cellular receptors, therefore determine metabolic fate of lipoprotein

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10
Q

What is ApoE synthesised by and involved in ?

A
  • Synthesised by the liver, brain, adipose tissue, and arterial wall
  • Most abundant in plasma lipoproteins derived primarily from the liver i.e. VLDL and LDL
  • Involved in the homeostasis of triacylglycerol-rich lipoproteins and HDL
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11
Q

In humans, ApoB48 is produced only in ?

A

The small intestine in response to fat in the diet

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12
Q

What is required for proper folding of ApoB proteins ?

A

Cholesterol esters

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13
Q

Only ApoB100 binds to?

A

ApoB specific receptors

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14
Q

What does ApoB-100 control vs ApoB-48 ?

A

ApoB-100 controls metabolism of LDL whereas ApoB-48 controls chylomicrons

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15
Q

ApoE controls ?

A

Receptor binding of remnant particles

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16
Q

ApoC act as ?

A

Enzyme activator/inhibitor & is extensively exchanged between different lipoprotein classes

17
Q

What are key determinants for VLDL and LDL formation?

A

ApoB100 and ApoE

18
Q

What happens without ApoB100 ?

A
  • Much less CHY, VLDL and LDL are formed and the plasma TAGs and cholesterol
    concentrations decrease as a result
19
Q

What is Hypothyroidism ?

A
  • An underactive thyroid gland
  • Common signs are tiredness and weight gain
  • Present in 1.4% to 13% of patients with hyperlipidemia
  • Overt hypothyroidism is a secondary cause of hyperlipidemia and associated coronary heart
    disease
  • Cholesterol profiles may be improved by treating overt hypothyroidism
20
Q

The lipid abnormalities seen with hypothyroidism are thought to be primarily related to ?

A

A reduction in LDL receptor activity

21
Q

Thyroid stimulating

hormone (TSH) might up-regulate ?

A

Hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) expression, which suggested a potential direct role of TSH in the cholesterol biosynthesis in the liver

22
Q

What can smoking do to the vessels, cholesterol levels and blood pressure?

A
  • Smoking can damage and tighten blood vessels, raise cholesterol levels, and raise blood pressure
  • Smoking also doesn’t allow enough oxygen to reach the body’s tissues