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ESA1 - Metabolism > Lipid Transport > Flashcards

Lipid Transport Flashcards

1
Q

Define the term ampiphatic

A
  • Both hydrophobic and hydrophilic properties e.g. Phospholipids
  • Polar and non-polar regions
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2
Q

Describe the formation of a MICELLE

A
  • Phospholipids coalesce in water to form a globular structure
  • Hydrophilic polar heads around the outside and hydrophobic non-polar tails on the inside
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3
Q

What is the difference between a MICELLE and a LIPOSOME?

A

Liposome is formed from a BILAYER of phospholipids (micelle is UNILAYERED)

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4
Q

Where does the cholesterol in our body originate from?

A
  • Obtained from diet

- Synthesised in the liver from HMG-CoA reductase

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5
Q

Why is cholesterol important?

A
  • Essential component of membranes (fluidity)
  • Precursor of steroid hormones
  • Precursor of bile acids
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6
Q

What is a cholesterol ester and how is it formed?

A
  • Cholesterol is transported around the body as cholesterol esters
  • Cholesterol molecule esterified with a fatty acid
  • Catalysed by CHOLESTEROL ACYLTRANSFERASE
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7
Q

List 3 components of a lipoprotein

A
  • Phospholipid monolayer (contains small amount of cholesterol)
  • Cargo containing TAGs, cholesterol esters and fat soluble vitamins
  • APOLIPOPROTEINS (peripheral on outside and integral which can pass through monolayer)
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8
Q

What are the 5 classes of lipoproteins?

A
  • Chylomicrons
  • VLDLs
  • IDLs
  • LDLs
  • HDLs
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9
Q

Which lipoproteins are the main carriers of FAT?

A
  • Chylomicrons

- VLDLs

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10
Q

Which lipoproteins are the main carriers of CHOLESTEROL ESTERS?

A
  • IDLs
  • HDLs
  • LDLs
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11
Q

How could you tell if chylomicrons were present in blood?

A
  • Form a ‘creamy layer’ on top of blood

- Usually only present up to 4-6hrs after a meal

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12
Q

What determines the density of the lipoprotein?

A
  • % protein content (more protein = more dense)

- diameter (smaller diameter = higher density as they are inversely proportional)

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13
Q

What are the structural and functional roles of apolipoproteins?

A
  • STRUCTURAL - packaging water insoluble lipid

- FUNCTIONAL - cofactors for enzymes; Ligands for cell surface receptors

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14
Q

How do chylomicrons enter the blood stream?

A
  • Loaded with Fats, cholesterol and vitamins in small intestine and enter lymphatic system
  • Travel to thoracic duct and enter blood through LEFT SUBCLAVIAN VEIN (avoids the liver)
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15
Q

When do chylomicrons acquire apoC and apoE apolipoproteins?

A

On entering the blood stream from the lymphatic system

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16
Q

What is the role of apoC in chylomicron metabolism?

A
  • Binds to LIPOPROTEIN LIPASE on adipocytes and muscle cells
  • Triggers the release of contents from chylomicron to the cells, depleting the fat contents of the chylomicron
  • TAGs can then be used by cells (either stored or metabolised)
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17
Q

What is a chylomicron remnant?

A

Formed when fat contents of chylomicron have been depleted to ~20% (emptied at muscle cells and adipocytes)

18
Q

What is the role of apoE in chylomicron metabolism?

A
  • apoE on chylomicron remnant binds to LDL receptor on hepatocytes and initiates receptor mediated endocytosis
  • Broken down by lysosomes and remaining fat content is released (used for metabolism)
19
Q

Where is lipoprotein lipase found?

A

Capillary walls of adipocytes and muscle cells

20
Q

How are LDLs formed from VLDLs?

A
  • VLDLs bind to lipoprotein lipase (LPL) at cells and deplete stores of TAGs
  • When stores deplete to ~30% -> becomes IDL particle
  • IDL further depletes stores of TAGs until ~10% where IDL loses apoC and apoE and becomes an LDL
  • LDL has a high cholesterol content
21
Q

Why do lipids need to be bound to carriers in order to me transported?

A
  • HYDROPHOBIC

- INSOLUBLE in water so cannot travel freely in blood

22
Q

Why do LDLs remain in the blood longer than other lipoproteins?

A
  • Do not have apoC or apoE so are not efficiently cleared by the liver
  • More susceptible to oxidative damage if they remain in blood
  • Oxidsied LDLs are taken up by macrophages to form foam cells —> atherosclerosis
23
Q

What is the main function of LDLs and how is this achieved?

A
  • Primary function is to provide cholesterol to peripheral tissues from liver
  • LDLs bind to LDL receptors on peripheral cells and are taken up by receptor mediated endocytosis
24
Q

What is RECEPTOR MEDIATED ENDOCYTOSIS?

A

Binding of ligand (e.g. apoB-100) of molecule (LDL) to cell surface receptor triggers the endocytosis of the molecule-receptor complex into cell in the form of an ENDOSOME

25
Q

Explain how receptor mediated endocytosis is used in the entering of LDL into cells

A
  • Cells express LDL receptor on plasma membrane
  • apoB-100 on LDL is a ligand for this receptor so binds to receptor forming RECEPTOR/LDL COMPLEX which then enters the cell by endocytosis
26
Q

State 3 ways in which HDLs can be synthesised

A
  • Nascent HDL syntheised in LIVER
  • “Bud off” from chylomicrons/VLDL as they are digested by LPL
  • Free apoA-1 can acquire cholesterol and phospholipids from other lipoproteins to form nascent-like HDL
27
Q

How do HDL particles mature?

A
  • Hollow core progressively fills as nascent HDL accumulate phospholipids and cholesterol from cells
  • Particle becomes more globular
  • Transfer of lipids to HDL does NOT require LPL
28
Q

What is the main role of HDLs?

A

Transport of EXCESS cholesterol from tissues to liver for disposal as bile salts or for cells that require additional cholesterol (steroidogenic cells)

29
Q

How do cells attain additional cholesterol from HDLs?

A
  • Utilise SCAVENGER RECEPTOR (SR-B1)

- Cholesterol used for steroid hormone synthesis

30
Q

Describe the action of cholesterol exchange transfer protein (CETP)

A

HDL can exchange cholesterol ester for TAGs with VLDL particles in blood

31
Q

What is the main role of VLDLs?

A

Transport of triacylglycerols (TAG) syntheised in liver to adipose tissue for storage

32
Q

What are the clinical signs of HYPERCHOLESTEROLAEMIA?

A
  • High level of cholesterol in blood

- Cholesterol deposits in various areas of body (e.g. eyelids, tendons, white circle around eye)

33
Q

Describe the formation of foam cells

A
  • LDL in blood becomes OXIDISED by ROS (lipid peroxidation)
  • Recognised by macrophages which engulf oxidised LDL
  • Macrophages become lipid-laden, forming foam cells
34
Q

Explain how the formation of an atherosclerotic plaque can lead to thrombosis

A
  • Foam cells accumulate in INTIMA of blood vessel wall forming a fatty streak which evolves into a plaque
  • Growth of plaque ENCROACHES lumen of vessel, restricting blood flow
  • Plaque RUPTURES, triggering acute thrombosis
35
Q

Explain the treatment methods for hyperlioproteinaemia

A
  • DIET modifications like reducing cholesterol and saturated fats; increasing fibre intake
  • LIFESTYLE changes e.g. More exercise, stop smoking
  • DRUG usage such as Statins and Bile Salt Sequestrants
36
Q

How do Statins help to reduce cholesterol?

A

Inhibit HMG-CoA reductase, an important enzyme in the synthesis of cholesterol from mevanolate

37
Q

What are the clinical consequences of atherosclerosis?

A

Encroaching of lumen of arteries can cause various diseases such as MI, STROKE and ANGINA

38
Q

Explain how increasing dietary fibre may help in lowering cholesterol

A
  • Interferes with reabsorption of bile salts in GI tract

- Liver is encouraged to make more bile salts, using cholesterol to do so

40
Q

Why might Statins cause side effects?

A
  • Inhibits HMG-CoA reductase (very early on in cholesterol synthesis)
  • Important intermediates produced during the synthesis of cholesterol cannot be formed
41
Q

What is the role of the ABCA1 protein?

A
  • REVERSE CHOLESTEROL TRANSPORT
  • Facilitates the transport of cholesterol from HDL particles inside cell
  • Cholesterol is converted to cholesterol esters using LCAT
42
Q

What is dyslipoproteinaemia?

A

Any defect in the metabolism of the plasma lipoproteins

43
Q

What characterises hyperlioproteinaemia?

A

Raised levels of one or more of the plasma lipoproteins

ESA1 - Metabolism (20 decks)

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