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CELL Yr 1 > Fat Transport > Flashcards

Fat Transport Flashcards

1
Q

How are free fatty acids transported in circulation?

A

Fatty acids circulate bound to protein to prevent them from having adverse effects on membranes (acting as detergents)

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2
Q

What’s the most common protein for fatty acids to be bound to?

A

Albumin

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3
Q

At what point does albumin become saturated with fatty acid?

A

2mM worth of fatty acid molecules

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4
Q

How can fatty acids enter cells?

A

Simple diffusion

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5
Q

What are the 5 types of lipoprotein?

A 
Chylomicrons
VLDL
LDL
IDL
HDL
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6
Q

What’s the name of the protein component of a lipoprotein?

A

Apolipoprotein or apoprotein

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7
Q

What are the 4 functions of apoproteins?

A

Maintain structural integrity
Solubilise lipids
Act as enzymes or enzyme cofactors
Tissue targeting

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8
Q

Describe the density of chylomicrons

A

Chylomicrons have the lowest density of the lipoproteins due to the fact they have high triglyceride content and low protein content.

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9
Q

How are chylomicrons secreted?

A

They’re secreted by reverse pinocytosis into the lymphatics

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10
Q

What’s the circulatory half-life of chylomicrons?

A

Around 30 minutes

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11
Q

What happens to chylomicrons as they pass through the circulation?

A

As chylomicrons pass through the circulation, triglycerides are removed and chylomicron remnants reach the liver before being removed

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12
Q

What causes the liver to take up the chylomicron remnants to be broken down or recycled?

A

Apo E binds to receptors in the liver to cause chylomicron remnant uptake?

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13
Q

What removes triglycerides from chylomicrons in circulation?

A

Lipoprotein lipase associated with endothelial cell membranes

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14
Q

How do lipoprotein lipase enzymes remove triglycerides from chylomicrons in circulation?

A

The lipoprotein lipase interacts with Apo C2 on the lipoprotein, activating the enzyme to degrade the lipoprotein into free fatty acids which can then diffuse into the cell.

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15
Q

What stimulates LPLs on adipocytes?

A

LPLs on adipocytes are stimulated by insulin

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16
Q

What is type 1 hyperlipidaemia?

A

Deficiency in lipoprotein lipase or Apo 2, characterised by high plasma triglycerides

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17
Q

What is type 2 hyperlipidaemia?

A

Characterised by high LDL; mostly caused by a genetic defect in the synthesis, processing or function of the LDL receptor

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18
Q

What is type 4 hyperlipidaemia?

A

The most common form results in raised VLDL concentrations, often due to obesity or alcohol abuse

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19
Q

Where are VLDLs synthesised?

A

The liver ER and golgi

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20
Q

What are VLDLs released with?

A

VLDLs are released with B100, then acquire Apo E and C from HDL

21
Q

What enhances formation of VLDLs?

A

Dietary carbohydrates, circulating FFA, alcohol and raised insulin and decreased glucagon

22
Q

What are LDLs the major carriers of?

A

Cholesterol

23
Q

How long does it take to metabolise LDLs?

A

3 days

24
Q

What do LDLs contain?

A

1 Apo B100 which can bind to a specific receptor on hepatocytes

25
Q

How are LDLs removed?

A

60% are removed by the liver, while 40% are removed by non-hepatic tissue (gonads or adrenal cortex) for steroid biosynthesis

26
Q

What are HDLs the circulating reservoir for?

A

Apolipoproteins (C2 and Apo E)

27
Q

Where are HDLs made?

A

HDLs are made in the liver and intestine, by budding from VLDL and chylomicrons, and from free Apo A1

28
Q

What’s the function of HDLs?

A

They remove cholesterol from plasma and dead or dying cells

29
Q

What’s the cholesterol removal process called?

A

Reverse cholesterol transport

30
Q

What does reverse cholesterol transport require?

A

A transporter called ABCA1, which interacts with the apolipoprotein to enable the transfer of cholesterol from the membrane into the lipoprotein for transport back to the liver, or exchange to other tissues

31
Q

What enzyme do HDLs contain?

A

Lecithin cholesterol acyltransferase (LCAT), which esterifies cholesterol

32
Q

Where does HDL bind to lipoproteins and cells via Apo E?

A

In the liver and steroid-producing cells

33
Q

What is a healthy HDL:LDL ratio?

A

3:5

34
Q

What can HDL:LDL ratio be used to assess?

A

Susceptibility to heart disease

35
Q

How are lipoproteins removed from circulation?

A

Receptor-mediated endocytosis.

36
Q

Describe receptor-mediated endocytosis

A

There are receptors on the cell surface which will bind to lipoproteins expressed by LDLs or HDLs. The consequence of that binding is that they form endosomes, and these endosomes are where the recycling of the receptor and the recycling of the lipoprotein’s contents takes place. The receptors can just be recycled and remain in the cytosol until they’re required at the cell surface. The components of the lipoprotein will then be broken down following union with lysosomes which contain all the hydrolytic enzymes that may break down proteins. Cholesterol esters release may be reincorporated into membranes. Amino acids and fatty acids can be used for metabolism

37
Q

What regulates cholesterol uptake and synthesis?

A

Cholesterol itself

38
Q

How does cholesterol reduce synthesis?

A

High cholesterol inhibits HMG-CoA reductase activity

39
Q

What does decreased cholesterol do?

A

Increases LDL receptor expression

40
Q

How do statins work?

A

Statins inhibit HMG-CoA, so low intracellular cholesterol increases LDL receptor expression at the cell surface, leading to increase uptake of LDL and lowered circulating LDL

41
Q

Where are LDL receptors found?

A

On LDL and VLDL in the liver

42
Q

What do LDL receptors bind to?

A

Apo B100

43
Q

Where are HDL receptors found?

A

On HDL, VLDL and chylomicrons in the liver

44
Q

What do HDL receptors bind to?

A

Apo E

45
Q

Describe scavenger receptors

A

They are low affinity, present on LDL, unregulated and found in endothelial cells, macrophages and VSMCs

46
Q

Describe familial hypercholesterolaemia

A

FH is caused by a single amino acid substitution that prevents localisation of the LDL receptor to the coated pits. Homozygous individuals have high serum cholesterol (4x normal), develop atherosclerosis, their de novo cholesterol synthesis isn’t regulated by LDL and they die young from heart attacks

47
Q

What regulates lipoprotein hormonally?

A

Insulin, cortisol and thyroid hormones

48
Q

How does diabetes mellitus affect lipid transport?

A

FFA mobilisation is increased and chylomicron and VLDL utilisation is decreased

49
Q

How does obesity affect lipid transport?

A

Hypertension, NIDDM, hyperlipidaemia and hyperglycaemia

CELL Yr 1 (13 decks)

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