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Lipids Flashcards

1
Q

Classes of lipids

A

Fatty acids - fuel
Triglycerides - fuel and insulation
Phospholipids - membranes and plasma lipoproteins
Eicosanoids - local mediators

Ketone bodies - water soluble fuel
Cholesterol - membranes and steroid hormone synthesis
Cholesterol esters - cholesterol storage
Bile acids and salts - lipid digestion

Vitamins A, D, E and K

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2
Q

Esterification

A

Glycerol + fatty acids -> triacylglycerol

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3
Q

Lipolysis

A

Triacylglycerol -> glycerol + fatty acids

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4
Q

Chylomicrons

A

Lipoprotein particle that transports dietary lipids in the blood.

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5
Q

Carnitine shuttle

A

Protein in inner mito. membrane that transports fatty acids across the membrane.

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6
Q

Fatty acid activation

A

In cytoplasm; fatty acids linked to CoA by fatty acrylic CoA synthase.

Fatty acid + ATP + CoA -> fatty acyl-CoA + AMP +2Pi

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7
Q

Fatty acyl CoA synthase

A

Activates fatty acids by linking to CoA in cytoplasm.

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8
Q

Carnitine shuttle transport across membrane

A

Acyl-CoA + carnitine -> acyl carnitine + CoA (in inter-membrane space)
Catalysed by CAT1.

Acyl carnitine transported through carnitine shuttle into matrix.

Acyl carnitine + CoA -> acyl-CoA + carnitine
Catalysed by CAT2.
(Fatty acid now on inside on mito.)

Carnitine returns via shuttle.

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9
Q

Regulation of carnitine shuttle

A

Levels of AMP and insulin - therefore this controls the rate of FA oxidation.

CAT1 is inhibited by malonyl-CoA.

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10
Q

Beta-oxidation

A

FA activated in cytoplasm by adding molecule of CoA.

Transport across mito membrane via carnitine shuttle.

Acyl-CoA molecule goes through two reactions, each removing 2 C, finally making acetyl-CoA.
=> feeds into TCA cycle

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11
Q

Where does beta-oxidation occur?

A

Most tissues and WBC, NOT brain and RBC.

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12
Q

How/where are ketone bodies generated?

A

The liver constantly generates ketone bodies from acetyl CoA; production much higher during fasting and starvation.

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13
Q

What is the normal plasma ketone body conc.?

What is the conc during starvation?

What is the conc in untreated type 1 diabetes?

A

<1mM

2-10mM

> 10mM

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14
Q

Ketogenesis

A

Production of ketone bodies

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15
Q

Why happens so that ketone bodies are made?

A

In the liver:
Low NAD+ substrate availability and NADH product inhibition cause TCA cycle to be inhibited, therefore acetyl-CoA is diverted from TCA cycle and made into ketone bodies.

Ketone bodies in blood now used by tissues - they take it in, convert into acetyl CoA, feed into TCA cycle.

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16
Q

Ketogenesis regulation

A

Fed state - insulin/glucagon ratio high
=> lyase inhibited + reductase activated -> cholesterol synthesis

Starvation - insulin/glucagon ratio low
=> lyase activated + reductase inhibited -> ketone body synthesis

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17
Q

Liposome

A

Vesicle with bilayer membrane of phospholipids

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18
Q

Micelle

A

Vesicle with single layer of phospholipids

19
Q

In what form is cholesterol transported around the body?

A

Cholesterol ester

20
Q

What is a lipoprotein?

A

Transport micelles with integrated proteins in their surface.

21
Q

What is a apolipoprotein?

A

Lipoproteins in the membrane of lipid transport vesicles.

22
Q

What does peripheral apolipoproteins mean?

Which two apolipoproteins are peripheral?

A

Peripheral proteins rest on top of the phospholipid bilayer.

ApoC, apoE

Further away from the start of the alphabet?

23
Q

What does integral apolipoproteins mean?

Which two apolipoproteins are integral?

A

Integral proteins pass through the phospholipid bilayer.

ApoA, apoB

At the start of the alphabet.

24
Q

What are the five classes of lipoproteins?

Name them in order according to density, lest to most dense.

A

Chylomicrons
VLDL (very low density)
IDL (intermediate)
LDL (low)
HDL (high)

25
What do lipoproteins contain? (4 things)
Apoliprotein Triglyceride Cholesterol Cholesterol ester
26
How long after a meal are chylomicrons present in the blood? How will chylomicrons make the blood plasma look?
4-6 hours after a meal. The plasma would appear creamy.
27
What are the 6 classes of apolipoproteins?
A, B, C, D, E, H
28
Roles of apolipoproteins
Structural: Packaging water insoluble lipid Functional: Co-factor for enzymes Ligands for cell surface receptors
29
What is the function of chylomicrons?
Transport dietary lipids
30
Lifecycle of a chylomicron, from small intestine to destruction
- loaded into the small intestine and apoB-48 added before entering lymph system - travel to thoracic duct which empties into left subclavian vein - acquires apoC and apoE once in blood - apoC binds lipoprotein lipase (LPL) on adipocytes and muscle - FA released into these cells, depleting chylomicron of fat content - when triglyceride reduced to 20%, apoC dissociates and chylomicron becomes chylomicron remnant - remnants return to liver - LDL receptor on hepatocytes binds apoE - remnant uptake taken up by receptor mediated endocytosis - lysosomes release remaining content for use in metabolism
31
Lipoprotein lipase
On capillary walls of muscle and adipose tissue; binds to apoC on chylomicrons. 2 lips around cock (LIPoprotein LIPase binds to apoC)
32
VLDL metabolism
- made in liver to transport TAG to tissues - apoB100 added during formation - apoC and apoE added from HDL particles in blood - VLDL binds to LPL on endothelial cells in muscle and adipose and starts to become depleted of TAG - in muscle - FA used for energy - in adipose - FA used for synthesis of TAG and stored as fat
33
Formation of IDL and LDL
VLDL -> IDL -> LDL
34
IDL and LDL metabolism
As TAG content of VLDL drops; Some VLDL’s dissociate from LPL and return to liver; If content of VLDL depletes to 30%, it becomes a short-lived IDL; IDL’s can be taken up by liver or rebind to LPL to further deplete TAG content; If content of IDL depletes to 10%, IDL loses apoC and apoE and becomes LDL particle with high cholesterol content. VLDL loses LPL -> IDL IDL loses apoC and apoE -> LDL (Vagina loses lips, becomes infertile Infertility loses cock and ejaculate, becomes limp)
35
Clinical relevance of LDLs in blood
Half life of LDL in blood is much longer than VLDL or IDL, making LDLs more susceptible to oxidative damage. Oxidised LDLs taken up by macrophage that transform into foam cells which become fatty streaks, and contribute to the formation of atherosclerotic plaques. => MI/stroke
36
How do LDLs enter cells?
Receptor mediated endocytosis - apoB-100 on LDL acts as ligand - LDL-receptors on plasma membrane - taken in by endocytosis - fuse with lysosomes for digestion
37
HDL metabolism
Slide 18 and 19
38
Hyperlipoproteinaemias Causes? Treatments?
Raised plasma level of one or more lipoprotein classes. Caused by either over-production or under-removal. Treat first by diet - reduce cholesterol and saturated lipids in diet. Lifestyle - increase exercise; stop smoking (reduce CVS risk) Treat next by drugs - statins - inhibit HMG-CoA reductase Bile salts equestrians - bind bile salts in GI tract
39
Hypercholesterolaemia Signs? (Hint - there are 3)
High levels of cholesterol in blood Deposits on areas of body: - xanthelasma - yellow patches on eyelids - tendon xanthoma - nodules on tendon - corneal arcus - white/bluish circle around eye (Corneal arcus in common in older people)
40
Keywords in LDL forming atherosclerosis
Oxidised LDL Macrophages Foam cells Fatty streak Atherosclerotic plaque Thrombosis Stroke/MI
41
What do statins inhibit?
HMG-CoA reductase
42
PCSK9 inhibitors - how do they work
PCSK9 promotes breakdown of LDL receptors in liver cells. They inhibit this protein => more LDL receptors recycled => more LDL particles removed from blood = lowers plasma cholesterol levels
43
Ideal total cholesterol in blood (TC)
5 mMol/L or less
44
Full cholesterol test levels - ideal levels
Total cholesterol - 5mMol/L or less Non HDL-cholesterol - 4mMol/L or less LDL-cholesterol - 3 mMol/L or less HDL-cholesterol - over 1mMol/L in men; over 1.2 mMol/L in women Total cholesterol:HDL-C - the lower the better (above 6 is considered high risk) Triglyceride - less than 2mMol/L in fasted sample

MEH (14 decks)

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