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Cardiovascular > Lipid metabolism > Flashcards

Lipid metabolism Flashcards

1
Q

What are the uses of lipids in the body?

A

Membrane biogenesis and membrane integrity, energy sources, precursors for hormones and signalling molecules.

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2
Q

How are non-polar lipids transported in the blood?

A

Within lipoproteins e.g. HDL and LDL.

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3
Q

What are the causes of elevated LDL and decreased HDL?

A

Diet and lifestyle, genetic factors e.g. familial hypercholesterolaemia.

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4
Q

What does the hydrophobic core of a lipoprotein contain?

A

Esterified cholesterol and triglycerides.

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5
Q

What is the hydrophilic coat of lipoproteins made from?

A

A monolayer of amphipathic cholesterol, phospholipids and one or more apoproteins.

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6
Q

What are the diameters of lipoproteins?

A

HDL: 7-20nm. LDL: 20-30nm. VLDL: 30-80nm. Chylomicrons: 100-1000nm.

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7
Q

What apoproteins do each type of lipoprotein have?

A

HDL: apoA1, apoA2. LDL and VLDL: apoB-100. Chylomicrons: apoB-48.

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8
Q

What are the function of apoB-containing lipoproteins?

A

Deliver triglycerides to muscle for ATP biogenesis and adipocytes for storage.

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9
Q

Describe the endogenous and exogenous pathway of apoB-containing lipoprotein formation.

A

Endogenous: VLDL particles formed in liver cells that transport triglycerides synthesised in that organ. Exogenous: chylomicrons formed in intestinal cells and transport dietary triglycerides.

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10
Q

What are the 3 stages in the life-cycle of an apoB-containing liposome?

A
  1. Assembly.
  2. Intravascular metabolism (involving hydrolysis of the triglyceride core).
  3. Receptor mediated clearance.
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11
Q

What kinds of lipids are transported passively into the enterocyte in the intestine?

A

Monoglycerides and free fatty acids (long chain).

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12
Q

What protein transports cholesterol into the enterocyte?

A

Niemann-pick C1-like 1 protein (NPC1L1).

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13
Q

What happens to the monoglycerides and free fatty acids in the enterocyte?

A

They are synthesised into triglycerides.

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14
Q

What processing does cholesterol undergo in the enterocyte?

A

Esterification to form a cholesteryl ester.

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15
Q

What process and enzyme leads to the production of a chylomicron in an enterocyte?

A

Lipidation and MTP (microsomal triglyceride transfer protein).

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16
Q

Where in the enterocyte are chylomicrons formed?

A

In the endoplasmic reticulum.

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17
Q

When will the chylomicron exit the enterocyte and how?

A

When a second apoproetin (apoA1) is added and by exocytosis.

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18
Q

How do chylomicrons enter the circulation?

A

They enter lymphatics and are carried in lymph to the systemic circulation (subclavian vein) via the thoracic duct.

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19
Q

Where are free fatty acids in the liver derived from?

A

Adipose tissue (particularly during fasting) and de novo synthesis.

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20
Q

Why and how are chylomicrons and VLDL particles activated?

A

To target triglyceride delivery to adipose and muscle tissue. Activated by transfer of apoCII from HDL particles.

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21
Q

What is LPL and where is it found?

A

Lipoprotein lipase , a lipolytic enzyme. In the endothelium of capillaries in adipose and muscle tissue.

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22
Q

How do VLDL and chylomicrons bind to LPL?

A

Through apoCII.

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23
Q

What does LPL do?

A

Hydrolyses core triglycerides into free fatty acids and glycerol which enter tissues.

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24
Q

What are chylomicron and VLDL remnants?

A

Particles depleted of triglycerides but still containing cholesteryl esters.

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25
Q

What do chylomicron and VLDL remnants exchange with HDL particles?

A

ApoCII transferred for apoE.

26
Q

What is apoE?

A

A high affinity for receptor mediated clearance.

27
Q

When the remnants return to the liver, what enzyme metabolises them further?

A

Hepatic lipase.

28
Q

What percentages of apoB48 and apoB100 remnants are cleared by receptor-mediated endocytosis into hepatocytes?

A

All apoB48, 50% of apoB100.

29
Q

What happens to the remaining apoB100-containing remnants?

A

Lose futher triglyceride through hepatic lipase, become small and enriched in cholesteryl ester. Via IDL become LDL particles lacking apoE and retaining solely apoB100.

30
Q

What is clearance of LDL mediated by?

A

LDL receptor expressed by the liver (and other tissues).

31
Q

What happens to the LDL once it is in the hepatocyte?

A

Cholesterol is released from cholesteryl ester by hydrolysis.

32
Q

What does released cholesterol in the hepatocyte cause?

A
  1. inhibition of HMG-CoA reductase which is the rate limiting enzyme in de novo cholesterol synthesis.
  2. Down regulation of LDL receptor expression.
  3. Storage of cholesterol as cholesteryl ester.
33
Q

What happens to LDL when it is uptaken into the intima of the artery in atherosclerosis?

A

It is oxidised to atherogenic oxidised LDL.

34
Q

What does the liver do with cholesterol and can other tissues eliminate it from the body.

A

Secretes it into bile or uses it to synthesise bile salts.

35
Q

Where is HDL formed and what is its first form?

A

In the liver, as apoA1 in association with a small amount of surface phospholipid and unesterified cholesterol (pre-beta-HDL).

36
Q

What shapes are pre-beta-HDL and alpha-HDL?

A

Pre-beta: disc-like. Alpha: spherical.

37
Q

How does pre-beta-HDL mature into alpha-HDL?

A

Surface cholesterol is enzymatically converted to hydrophobic cholesterol ester that migrates to the core of the particle.

38
Q

Why is HDL good cholesterol?

A

It removes excess cholesterol from cells by transporting it to the liver.

39
Q

What are the 2 mechanisms that HDL uses for reverse cholesterol transport?

A
  1. HDL reaching liver interacts with scavenging receptor-B1 (SR-B1) that allows transfer of cholesterol and cholesteryl ester into hepatocytes.
  2. Cholesteryl ester transfer protein (CETP) in plasma mediates transfer of cholesteryl esters from HDL to VLDL and LDL, indirectly returning cholesterol to the liver.
40
Q

What causes primary dyslipidaemia?

A

Combo of diet and other genetic factors.

41
Q

What causes secondary dyslipidaemia?

A

Other diseases e.g. type II diabetes, hypothyroidism, alcoholism, liver disease).

42
Q

Give 2 examples of statins.

A

Simvastatin and atorvastatin.

43
Q

If you have a high LDL, what is your drug of choice?

A

A statin.

44
Q

What enzyme are statins competitive inhibitors of?

A

HMG-CoA reductase

45
Q

What does HMG-CoA reductase mediate?

A

The rate limiting step in cholesterol synthesis in hepatocytes.

46
Q

Why is decrease in hepatocyte cholesterol synthesis a good thing?

A

It causes a compensatory increase in LDL receptor expression and enhanced clearance of LDL.

47
Q

What are the other beneficial effects of statins?

A

Decreased inflammation, reversal of endothelial dysfunction, decreased thrombosis, stabilisation of atherosclerotic plaques.

48
Q

What time of day should you take a statin?

A

At night.

49
Q

When is the incidence of side effects of statins increased?

A

When administered with a fibrate.

50
Q

When would you use a fibrate?

A

In patients with very high triglyceride levels.

51
Q

Give 2 examples of fibrates.

A

Bezafibrate and gemfibrozil.

52
Q

What is the mechanism of action of fibrates?

A

Agonists of a nuclear receptor (PPARalpha) to enhance the transcription of several genes including that encoding LPL.

53
Q

Give 3 examples of bile acid binding resins.

A

Colestyramine, colestipol, colsevelam.

54
Q

How do bile acid binding resins work?

A

Cause excretion of bile salts resulting in more cholesterol to be converted to bile salts by interrupting enterohepatic recycling. (prevent reabsorption of bile salts in GI tract).

55
Q

How are bile acid binding resins taken and what is their adverse effect?

A

Orally, GI tract irritation.

56
Q

What does ezetimibe inhibit and what is the effect of this?

A

Inhibits niemann-pick C1 like-1 (NPC1L1) transport protein in enterocytes of the duodenum, reduces absorption of cholesterol.

57
Q

What is ezetimibe’s effect on LDL and HDL?

A

Decreases LDL, doesn’t change HDL.

58
Q

When is ezetimibe used?

A

In combo with statins when statins alone do not achieve a sufficient response.

59
Q

How is ezetimibe administered and why does it have a long half-life (22 hours)?

A

Orally. Metabolised to active metabolite that undergoes enterohepatic recycling.

60
Q

What are the potential adverse effects of ezetimibe?

A

Diarrhoea, abdominal pain and headache.

61
Q

When shoud ezetimibe not be used?

A

In pregnant women.

Cardiovascular (32 decks)

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