Lecture 4 Flashcards

Question

Where do VLDL’s go if content is above 30%?

Answer 1

-LPL dissociates from VLDL and complex can return to liver

Answer 2

LDL - provide cholesterol from liver to peripheral tissues - peripheral cells express LDL receptors and take up LDL via receptor mediated endocytosis, LDL’s can also be reuptaken by liver via same mechanism to release cholesterol/TAG’s - responsible for formation of atherosclerotic plaques in atherosclerosis

Answer 3

Below 30%: - Formation of IDL particle (short lived) - IDL particles can be depleted further by rebinding to LPL/taken back to liver - if IDL becomes depleted to 10% of original content - IDL loses apoC & apoE becoming an LDL (high cholesterol content)

Answer 4

- Have a very long half life, making them more susceptible to oxidative damage via lipid peroxidation - oxidised LDL taken up by macrophages forming FOAM cells, contributing to atherosclerotic plaques - don’t have apoC/apoE so not efficiently cleared by the liver,as hepatocytes have LDL receptor which bind to apoE

Answer 5

Receptor mediated endocytosis. - cells requiring cholesterol express LDL receptors - apoB100 on LDL acts as ligand for those receptors - endocytosis forming and endocytic vesicle - vesicle fuses with lysosome and contents degraded - the LDL receptor is degraded or recycled back to cell surface

Answer 6

- synthesised by liver OR bud off from chylomicrons/VLDL OR formed from apoA-1 - empty/low levels of TAG

Answer 7

-they can acquire cholesterol + phospholipid from other lipoproteins and cell membranes to form HDL’s

Answer 8

Remove extra cholesterol that cells may have (reverse cholesterol uptake) - accumulate phospholipids and cholesterol - particle becomes more globular - doesn’t require enzymes

Answer 9

- HDL’s remove cholesterol - important for blood vessels as reduces likelihood of foam cells and plaque formation - ABCA1 protein within cell allows transfer of cholesterol into the HDL particles - cholesterol converted to cholesterol ester via LCAT

Answer 10

LDL carrying cholesterol is bad- leads to atherosclerosis formation HDL carrying cholesterol is good- removes excess cholesterol from cells and returns it back to the liver

Answer 11

- taken up by liver via receptors - cells requiring additional cholesterol e.g. steroidogenic cells to make steroid hormones, utilise SCAVENGER receptor (SR-B1) to obtain cholesterol from HDL’s - the excess cholesterol once entered into the liver, can be used to make bile

Answer 12

They can exchange a cholesterol ester for TAG with VLDL/LDL via cholesterol exchange transfer protein (CETP)

Answer 13

``` Raised plasma level of one or more lipoprotein classes. Caused by: -over-production -under-removal Defects in: -enzymes -receptors -apoproteins ```

Answer 14

6 main classes

Answer 15

High level of cholesterol in blood- causing deposits of cholesterol to form - Yellow patches on eyelid (Xanthelasma) - Nodules on tendon (tendon xanthoma) - Corneal arcus- white Circe around eye. Common in elderly, not in young so could indicate hyperchoesterolaemia

Answer 16

Raised serum LDL - oxidised LDL: lipid inside becomes oxidised (due to longer half life) - oxidised LDL particle is recognised by macrophages and engulfed - macrophages become laden with lipid forming FOAM CELLS - foam cells accumulate in the intima (innermost layer) of the blood vessel walls forming a fatty streak - fatty streaks can evolve into an atherosclerotic plaque - plaques can grow and restrict lumen

Answer 17

In coronary artery: -angina (plaque blocking blood flow, lack of oxygen to myocardium) Plaque ruptures -thrombus forms (clot) activating platelets, block entire artery (In coronary artery= MI, in brain artery = Stroke) -promotes smooth muscle growth so tunica media gets larger also

Answer 18

1st approach: - diet (reduce cholesterol & saturated lipids, increase fibre intake) - lifestyle (increases exercise & stop smoking- remove oxidative stress) 2nd approach: - Statins ( reduce synthesis of cholesterol, by inhibiting HMG-CoA) e.g.atorvastatin - bile salt sequestrants (bind bile salts in GI tract: forces liver to make more bile acids using more cholesterol) e.g.colestipol

Answer 19

Inhibit HMG-CoA reductase -catalyses HMG-CoA to mevalonate Acetyl-CoA > HMG-CoA > mevalonate >>>squalene>>>cholesterol

Answer 20

Because the statin blocks the synthesis of cholesterol strongly and early on so the other metabolites produced in the synthesis are also not produced.

Answer 21

4 mmol/L or less

Answer 22

3 mmol/L or less

Answer 23

Over 1/1.2 mmol/L

Answer 24

Less than 2 mmol/L

Answer 25

RNA editing. ApoB-100 is the full size -RNA from apoB-100 is edited to produce an early stop codon= 48% of original size

Answer 26

Chylomicrons contain apoB-48 | VLDL’s contain apoB-100

Answer 27

To bypass fast metabolism by the liver.

Lecture 4 Flashcards

(51 cards)