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MEH Sem1 > Lipids > Flashcards

Lipids Flashcards

1
Q

Are lipids more or less reduced that carbohydrates?

A

More reduced - so when oxidised they release more energy but this requires more 02

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2
Q

What are the 3 classes of lipids and give an example of each?

A
  1. Fatty acid derivatives e.g. fatty acids and TAGs, phospholipids
  2. Hydroxy-methyl-glutamic acid derivative (C6 compound) e.g. ketone bodies and cholesterol and bile acids and salts
  3. Fat soluble vitamins - ADEK
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3
Q

Where and how are TAGs stored?

A

They are stored in adipose tissues in anhydrous forms because they are hydrophobic.

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4
Q

Describe dietary TAG metabolism

A
  1. Lipids = fatty acids and glycerol
    In SI converted into TAG again in GI tract.
  2. Packaged into chylomicron, a lipoprotein particle - helps to stabilise the, during transport
  3. Released into general circulation in lymphatics and taken to adipose tissues and stored as triglycerol.
  4. When needed, FA released and carried to tissues as an albumin-FA complex.
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5
Q

How are FA’s catabolised?

A

FA acids activatedd by linking to CoA via Fatty acyl-coA synthase. Then transported across inner mitochondrial membrane via carnitine shuttle - this overcomes the fact that mitochondria is normally impermeable to FA.

Then various beta oxidative pathways where they lose a C2 each time. Reducing power generated. Then the C atoms of the fatty acids are converted to Acetyl-CoA to be used in other metabolism.

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6
Q

How is beta oxidation of fatty acids regulated?

A

Regulated by AMP and insulin
CAT1 inhibited by malonyl-CoA

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7
Q

Where does beta oxidation of fatty acids not occur?

A

The brain as FA can’t cross the BBB and also the RBC as no mitochondria.

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8
Q

How is the glycerol from TAGs metabolised?

A

TAGs broken down by pancreatic lipase in small intestine into FA and glycerol phosphate. This can be converted to Dihydroxyacetone phosphate and enter glycolysis as Glyceraldehyde 3P.
Glycerol phosphate to DHAP is catalysed by glycerol-3-phosphate dehydrogenase.
Lipid synthesis in adipose tissue needs glycolysis but the liver can directly phosphorylase glycerol.

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9
Q

What is the pKa of ketone bodies?

A

4 - makes the blood acidic

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10
Q

What are the 3 ketone bodies made in the body?

A

Acetone - not used as a fuel source
Acetoacetate
B-hydroxybutyrate

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11
Q

How do statin drugs work?

A

They prevent the formation of cholesterol from mevalonate from acetyl-coA by inhibiting the action of HMG-CoA reductase.

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12
Q

How is the production of ketone bodies regulated by the liver?

A

Increased by a low NAD+ status, or if the production of NADH inhibited (via isocitrate dehydrogenase or a-ketoglutarate dehydrogenase) because this inhibits the TCA cycle so shifts towards ketone body production.

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13
Q

How is ketone body synthesis regulated by insulin and glucagon in the fed state vs the starvation state?

A

When ratio is high in the fed state lease is inhibited and HMG-coA reductase is activated leading to cholesterol synthesis.

When ratio is low, lyase activated and reductase inhibited so moves towards ketone body synthesis.

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14
Q

Summarise how acetyl coA production ends with either cholesterol or ketone bodies

A

Acetyl-CoA is converted to HMG-CoA.
If in the fed state - cholesterol produced.
If in the starvation state - ketone bodies produced for use in muscle tissues.

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15
Q

How are lipids carried in the blood?

A

2% as albumin bound - usually FA

98% lipoprotein bound

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16
Q

What is the average amount of lipids in grams per litre of blood?

A

4-8.5g/L blood

17
Q

Where does cholesterol come from, how is it transported and what are some of its uses?

A

Some from diet but most from liver. It is transported as a cholesterol ester with a fatty tail added and then in a lipoprotein.

Uses:
- membrane structure
- precursor in steroid hormone e.g. oestrogen and testosterone
- precursor of bile salts

18
Q

What are lipoproteins?

A

Soluble proteins that transport lipids around the blood. They can take various structures e.g. a micelle with a phospholipid monolayer. You can get peripheral and internal types of lipoproteins. There are 5 different types.

19
Q

What are the 5 different classes of lipoproteins?

A
  1. Chylomicrons - for dietary fats (largest in size)
  2. VLDL
  3. IDL
  4. LDL ‘bad cholesterol’
  5. HDL ‘good cholesterol’ - transports excess cholesterol from cells to the liver (smallest in size - high % protein)

Particle size inversely proportional to their density.

1 and 2 = main carrier of fats
3-5 = main carriers of cholesterol esters

20
Q

How long are chylomicrons typically in the blood for after eating?

A

4-6hrs post eating

21
Q

How is lipoprotein density measured?

A

Via flotation ultracentrifugation

22
Q

What are apolipoproteins and what are their functions?

A

They are a particular class of proteins associated with each lipoprotein particle. They can be integral or they can be peripheral.

They help to package the lipid and they also are co-factors for enzymes and act as ligands for cell surface receptors.

23
Q

How are chylomicrons metabolised?

A

They are loaded in small intestine and the ApoB-48 alipoprotein is added.
Chylomicrons travel to thoracic duct to left subclavian vein and ApoC and ApoE added once in the blood.

ApoC binds lipoprotein lipase on muscle and adipocyte cells and this causes release of the FA into the cell.
when TAG reduced to 20%, the ApoC dissociates from chylomicron and it becomes a chylomicron remnant. These return to the liver . LDL receptor on hepatocyte binds ApoE & remnant taken up by receptor mediated endocytosis. Contents released from lysosome for metabolism.

24
Q

Describe VLDL metabolism?

A

Made in liver to transport TAGs to other tissues. ApoB100 added when formed and ApoC and E added from HDL particles in blood.

VLDL binds to lipoprotein lipase on endothelial cells In muscle and adipose tissue and start to become depleted of TAGs.

25
Q

How are fatty acids used in the muscle vs in the adipose tissue?

A

Muscle - released FA taken up from VLDL and used for energy production

Adipose - FA used to re-synthesise TAG and stored as fats

26
Q

How is IDL and LDL metabolism linked to VLDL?

A

When TAG content of VLDL drops some particles dissociate from the Lipoprotein lipase enzyme complex and go back to liver. If VLDL content depletes to around 30% this becomes a short lived IDL particle. These can also then be taken up by the liver or rebind you LPL enzyme to further deplete TAG content.

Depletion go to around 10% - IDL loses ApoC and ApoE and becomes an LDL particle with a high cholesterol content.

27
Q

What is the function of LDL and IDL?

A

LDL - provide cholesterol to tissues from liver - taken up via receptor mediated endocytosis.

LDL does not have ApoC or ApoE so not cleared well by the liver so has a much longer half life and more likely to get oxidatively damaged.

If they get damaged they are taken up by macrophages that can transform the, to foam cells, make a fatty streak then form artherosclerotic plaques. = bad cholesterol

28
Q

How do LDL enter cells?

A

By receptor mediated endocytosis. Cells that need cholesterol express LDL receptors on their membrane and the apoB100 on LDL acts as a ligand for receptors.
Taken into cell by endocytosis into endosome and fuses with a lysosome to digest contents to release cholesterol and FA.

29
Q

How is the LDL receptor expression on cells controlled?

A

By the concentration of cholesterol in the cell

30
Q

Describe HDL metabolism

A

New HDL synthesised in liver in response to low TAG levels. Can also bud off of chylomicrons and VLDL during digestion by LPL.

These accumulate phospholipids and cholesterols from cells lining blood vessels and they fill with TAG until the form a globular shape. Does not need an enzyme

Can also return cholesterol to liver by taking it from cells that are burdened. Reduces likelihood of foam cells and artherosclerotic plaques in blood vessels.

Mature HDL taken up by liver.
Cells that need cholesterol can scavenge it from HDL (SR-B1).
HDL can also exchange cholesterol ester for TAG with VLDL via cholesterol exchange transfer proteins.

31
Q

How is cholesterol transferred to HDL from cells?

A

ABCA1 protein facilitates the cell transferring cholesterol to HDL. Then it is converted to cholesterol ester.

32
Q

What is the importance of free apoA-I in HDL metabolism?

A

Free apoA-I can acquire cholesterol and phospholipids fro, other cell membranes and lipoproteins to form new HDL

33
Q

What are the main functions of each lipoprotein?

A

Chylomicron-dietary TaG transport
to adipose and muscle tissue

VLDL transport of TAGs synthesised in liver to adipose tissue

IDL and LDL - transport of cholesterol synthesised in liver to tissues

HDL - transport of excess cholesterol from cells to liver to be removed as bile salts or also transfer of cholesterol to cells needing it e.g. steroid formation

34
Q

What is hyperlipoproteinaemias?

A

Increased levels of one or more lipoprotein the blood caused by either under excretion or over production. 6main classes caused by defects in either enzymes, receptors or apoproteins.

35
Q

What are the 3 main clinical signs of hypercholesterolaemia visisble on an individual?

A

Cholesterol deposits on body:
1. Xanthelasma - yellow patches on eyelids

  1. Tendon Xanthoma - nodules on tendons of knuckles
  2. Corneal Arcus - blue/white circle around eye, common in older ppl anyway but concerning in young
36
Q

How do you treat hyperlipoproteinaemias?

A

Diet first - reduce cholesterol and saturated fats. Increase fibre to promote excretion. Stop smoking, increase exercise.

Medication - statins to reduce synthesis of cholesterol by inhibiting HMG-CoA reductase

Bile salts sequestrants - bind bile salts to force liver to produce more and use up stored cholesterol e.g. Colestipol

37
Q

What is the clinical importance of PCSK9 inhibitors?

A

PCSK9 Promotes breakdown of LDL receptors on liver cells.
Inhibiting this means more LDL receptors present and more LDL recycled e.g. Inclisiran.

38
Q

What are the normal levels of total cholesterol and triglyceride in the blood?

A

Total cholesterol less than 5mmol/L

Triglycerides less than 2mmol/L in fasted sample

MEH Sem1 (6 decks)

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