Lipids Flashcards

1
Q

Which lipids of HMG derivatives?

A

ketone bodies, cholesterol, bile acids and salts

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2
Q

What are the fat soluble vitamins?

A

A, D, E and K

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3
Q

Which molecule can transport fatty acids in the blood?

A

Albumin

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4
Q

When are TAGs utilised?

A

exercise, starvation and pregnancy

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5
Q

Which enzyme mobilises TAG?

A

Hormone sensitive lipase

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6
Q

What does it mean that TAG is stored in a dynamic state?

A

TAG is constantly being formed and broken down.

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7
Q

How are fatty acids activated?

A

linking to coenzyme A by fatty acyl coA synthase
investment of ATP
in cytoplasm

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8
Q

Which membrane is the carnitine shuttle on?

A

The inner mitochondrial membrane

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9
Q

Why is the carnitine shuttle needed?

A

Because coenzyme A is too big to cross the inner mitochondrial membrane

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10
Q

How does the carnitine shuttle work?

A

Carnitine is combined with acyl and the coA is released. Acyl carnitine is transported across the inner mitochondrial membrane via the shuttle. Acyl carnitine is broken down to reform acyl coA.

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11
Q

Which enzyme is required for the carnitine shuttle?

A

Carnitine acyltransferase

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12
Q

Which molecule inhibits the carnitine shuttle?

A

Malonyl-coA

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13
Q

What can defects in the shuttle system cause?

A

exercise intolerance and lipid droplets in muscle

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14
Q

Where does beta oxidation not occur and why?

A

brain, RBCs and WBCs
Brain = fatty acids cannot cross the blood brain barrier
cells = do not have mitochondria

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15
Q

How does beta oxidation work?

A

The removal of 2 carbons per cycle. Hydrogen is transferred to NAD+ and FAD. There is no ATP synthesis and the process stops in the absence of oxygen.

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16
Q

Where is glycerol metabolised?

A

Liver

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17
Q

Which enzyme activates glycerol and what is the product?

A
enzyme = glycerol kinase
product = glycerol phosphate
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18
Q

What can glycerol phosphate be used for?

A

TAG synthesis or DHAP synthesis

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19
Q

Name the 3 ketone bodies

A

acetoacetate, acetone and beta-hydroxybutyrate

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20
Q

Where are ketone bodies synthesised?

A

Mitochondria in the liver

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21
Q

Which enzyme needs to be activated for ketone body synthesis?

A

HMG-CoA Lyase

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22
Q

Which enzyme is inhibited during ketone body synthesis?

A

HMG-CoA Reductase

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23
Q

Which hormone activates HMG-CoA lyase?

A

Glucagon

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24
Q

Are ketone bodies water soluble?

A

Yes

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25
Q

What happens to fatty acids with an odd number of carbon atoms?

A

beta-oxidation until a 3 carbon molecule is formed
carboxylation to methyl malonyl coA
rearranged to succinyl coA (vitamin B12 cofactor)

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26
Q

Which lipids are fatty acid derivatives?

A

TAGs and phospholipids

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27
Q

How are lipids transported in the blood?

A

Fatty acids can be bound to albumin. However 98% of lipids are carried as lipoprotein particles.

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28
Q

What value should plasma cholesterol be below?

A

5mmol/L

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29
Q

What is the difference between a micelle and a liposome?

A
Micelle = one layer of phospholipids
Liposome = bilayer of phospholipids
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30
Q

Where does cholesterol come from?

A

some in the diet but most synthesised by liver

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31
Q

What is cholesterol a precursor to?

A

steroid hormones and bile acids

32
Q

How is cholesterol transported?

A

As cholesterol ester.

Cholesterol + fatty acid

33
Q

What are the main carriers of fat?

A

chylomicrons and VLDLs

34
Q

What are the main carriers of cholesterol esters?

A

ILDL, LDL and HDL

35
Q

Which lipoprotein particle has the biggest diameter?

A

Chylomicron

36
Q

Which lipoprotein particle has the smallest diameter?

A

HDL

37
Q

How many classes of apolipoproteins are there?

A

6 major classes

38
Q

Name the major classes of apolipoproteins

A

A, B, C, D, E and H

39
Q

What are the roles of apolipoproteins?

A

maintain structural integrity, cofactor for enzymes and ligand for receptors

40
Q

Where are chylomicrons loaded?

A

In the small intestine

41
Q

What is the pathway for chylomicrons?

A

loaded in small intestine, enter lymphatic system, travel to thoracic duct, enter left subclavian vein, bind to lipoprotein lipase on adipocytes and muscle, release fatty acids, become chylomicron remnant then return to liver to be broken down

42
Q

Which apolipoproteins do chylomicrons gain once they enter the blood?

A

apoC and apoE

43
Q

Which apolipoprotein of chylomicrons binds to lipoprotein lipase?

A

apoC

44
Q

When does a chylomicron become a remnant?

A

When TAG ~ 20% and apoC dissociates

45
Q

What does apoE bind to?

A

LDL receptor on hepatocytes

46
Q

What is the role of lipoprotein lipase?

A

Hydrolysis of TAG

47
Q

Where and why is VLDL made?

A

Liver

Transport TAG

48
Q

Which apolipoproteins does VLDL have and where are they added?

A

apoB100 - added in liver

apoC and apoE - added in blood

49
Q

When does a VLDL become an IDL?

A

when the content is ~30%

50
Q

What happens when IDL content is ~10%?

A

IDL loses apoC and apoE

becomes an LDL particle

51
Q

What is the primary function of LDL?

A

Transport cholesterol from liver to tissues

52
Q

What is the difference between LDL and IDL/VLDL?

A

LDL does not have apoC or apoE and therefore is not efficiently cleared by the liver.

53
Q

What is receptor expression for a lipoprotein particle controlled by?

A

cholesterol content within the cell

54
Q

Which of VLDL, IDL or LDL has the longer half life?

A

LDL has a longer half life

55
Q

How are atherosclerotic plaques formed?

A

oxidised LDLs are taken up by macrophages
Enter into the tunica intima
transform into foam cells
form plaques

56
Q

Where is HDL synthesised?

A

liver and intestine

57
Q

Which lipoprotein particles can HDL bud off?

A

VLDL and chylomicrons

58
Q

How does HDL fill up?

A

HDL accumulates phospholipids and cholesterol from cells lining blood vessels
hollow core fills
ABCA1 protein facilitates transfer of cholesterol to HDL

59
Q

Which enzyme converts cholesterol to cholesterol ester?

A

LCAT

60
Q

What is the function of chylomicrons?

A

transport dietary TAG from intestines to tissues

61
Q

What is the function of VLDL?

A

transport of TAG synthesised in liver to adipose tissue

62
Q

What is the function of IDL?

A

Precursor of LDL. Transport of cholesterol synthesised in the liver to tissues.

63
Q

What is the function of LDL?

A

Transport of cholesterol synthesised in the liver to the tissues.

64
Q

What is the function of HDL?

A

Transport of excess cholesterol from tissues to liver for disposal as bile salts.

65
Q

What is a hyperlipoproteinaemia?

A

A raised plasma level of one of more lipoprotein class.

66
Q

What causes Type I hyperlipoproteinaemia and how would you spot it?

A

defective lipoprotein lipase

chylomicrons present in fasting plasma sample

67
Q

What causes Type IIa hyperlipoproteinaemia and what is it also called?

A

defective LDL receptor

familial hyperlipoproteinaemia

68
Q

What are the clinical signs of hypercholesterolaemia?

A

high cholesterol in blood and cholesterol depositions

69
Q

Where can cholesterol depositions occur?

A

eyelids, tendons and eyes

70
Q

Which layer do foam cells build up in?

A

Tunica intima

71
Q

How do you treat hyperlipoproteinaemias?

A

change diet: reduce cholesterol, reduce fats, increase fibre
increase exercise
stop smoking
take statins - reduce cholesterol synthesis
take bile salt sequestrants - liver must produce more bile salts and therefore use up more cholesterol

72
Q

Why should a patient with hyperlipoproteinaemia increase their fibre intake?

A

More fibre means that the liver will make more bile salts and therefore more cholesterol is removed from the blood.

73
Q

What is the problem with statins?

A

They have many side effects because they inhibit cholesterol synthesis early on in the process.

74
Q

Why might a low protein diet affect lipid transport?

A

The liver cannot synthesise sufficient apolipoproteins to export the TAG it synthesises. Fatty liver may occur.

75
Q

Define emesis

A

Vomiting

76
Q

Define oedema

A

Increased net flow of fluid from plasma to tissues because of reduced oncotic pressure.