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M103 T3 > M103 T3 L15 > Flashcards

M103 T3 L15 Flashcards

1
Q

What are the two major metabolic pathways for what happens to TGs?

A

oxidation

synthesis

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2
Q

What happens at the end of FA oxidation?

A

the TG mlcs are oxidised in the mitochondria

E is released (ATP)

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3
Q

How does FA synthesis occur?

A

excess acetyl-CoA is joined to a glycerol molecule for storage

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4
Q

What are the three stages of the FA oxidation? (BroKE)

A

1- β-oxidation
2- the krebs cycle
3 - e- transfer (ETS)

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5
Q

What happens during the β-oxidation stage of FA oxidation?

A

the glycerol backbone is removed

the long chain FAs are oxidised

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6
Q

What are FAs oxidised into?

A

water and co2

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7
Q

What are the long chain FAs oxidised into during the β-oxidation stage?

A

acetyl-CoAs (2C fragments)

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8
Q

What happens during the Krebs Cycle stage of FA oxidation?

A

acetyl-CoA (from the β-oxidation stage) is oxidised into co2

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9
Q

What happens during the ETS of FA oxidation?

A

e-s generated in the Krebs cycle are transported on reduced e-carriers, and transferred to the Mitochondrial Respiratory Chain

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10
Q

What are the stages of β-oxidation of FAs? (FA’R AC)

A

FA activation
the Rate Limiting Step
acetyl CoA generation

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11
Q

Where does β-oxidation of FAs occur?

A

mitochondria

peroxisomes

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12
Q

How are FAs activated in the first stage of β-oxidation?

A

they are attached to CoA in the cytosol

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13
Q

What happens to acyl-groups during the Rate Limiting step during β-oxidation?

A

they’re transferred in across the mitochondrial membrane

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14
Q

Which CARrier proTEIN Transfers acyl-groups across the mitochondrial membrane during the rate limiting step?

A

carnitine

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15
Q

Where is carnitine located?

A

in the inner membrane of the mitochondria

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16
Q

What is the drawn out formula for the activated acyl group?

A

R - C (= O) - SCoA

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17
Q

What is the drawn out formula for the acyl group?

A

R - C = O

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18
Q

How does carnitine transport the activated acyl group into the mitochondria’s matrix?

A

by binding to the FA part of the mlc - only this part is transported across, the acyl group itself is left behind
AAR, there are two pools of CoA - one in the cytosol and one in the matrix

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19
Q

What happens to the acyl groups once they have been transferred into the matrix of the mitochondria?

A

they are again joined to a CoA mlc

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20
Q

What is the overall outcome of the rate limiting step?

A

acyl groups are transferred across the mitocondrial membrane into the mitochondria
the rate of beta oxidation is limited

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21
Q

Which two enzymes control the rate limiting step?

A

carnitine palmitoyl transferase I & II

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22
Q

Once inside the mitochondria, what happens next to the FAs?

A

the third step of β-oxidation of FAs

acetyl CoA generation

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23
Q

How is acetyl CoA generated?

A

FAs in the mitochondria undergo progressive oxidation

2-Cs are removed, leaving acetyl-CoA

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24
Q

What happens to acetyl-CoA once generated?

A

it enters the Krebs cycle

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25
Q

Where does FA synthesis mainly occur in the body?

A

in the liver and in adipocytes

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26
Q

How does FA synthesis occur?

A

long C chain molecules built up from 2-C units derived from acetyl CoA

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27
Q

Where does FA synthesis mainly occur in the cell?

A

in the cytosol

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28
Q

What does the citrate malate cycle allow to occur?

A

acetyl-CoA to be transported from the mitochondria into the cytosol so that FA synthesis can occur

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29
Q

What happens during the citrate malate cycle?

A

acetyl-CoA + OAA = citrate

citrate is moved out of the mitochonria into the cytosol by a tricarboxylate transporter

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30
Q

What happens to the citrate once it is in the cytosol at the end of the citrate malate cycle?

A

it is converted back into OAA and acetyl-CoA

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31
Q

What happens to the OAA in the cytosol after the citrate malate cycle has taken place?

A

it is converted via malate to pyruvate
transported back into the cell
used again to generate acetyl-CoA

32
Q

What is acetyl-CoA converted to when in the cytosol?

A

malonyl CoA

33
Q

What is the relationship between acetyl-CoA and malonyl CoA?

A

the more acetyl-CoA, the more malonyl CoA is formed

and the more FA biosynthesis will occur

34
Q

What is the role of FA synthase enzyme?

A

binds to malonyl CoA and acetyl-CoA

it joins molecules of acetyl-CoA together to build up FAs

35
Q

What is the rate limiting step for FA synthesis?

A

the formation of malonyl-CoA from acetyl-CoA

36
Q

What is the role of acetyl CoA carboxylase?

A

to convert acetyl-CoA into malonyl-CoA

37
Q

What hormones regulate acetyl CoA carbolxylase and HMG-CoA Reductase?

A

glucagon

insulin

38
Q

What functions do bile salts help in?

A

lipid digestion and absorption

cholesterol excretion

39
Q

What substance is cholesterol synthesised from?

A

acetyl-CoA

40
Q

What substance excretes cholesterol from the body?

A

bile acids

41
Q

What is the storage form of cholesterol?

A

cholesterol ester (found in most tissues)

42
Q

Which atoms make the cholesterol molecule ampipathic?

A

the -OH group on the end

43
Q

Which atoms make the cholesterol ester molecule hydrophobic?

A

the FA group on the end
R - C (= O) - O
where the -OH group was

44
Q

What is the role of cholesterol acyltransferases?

A

the esterification of cholesterol to cholesterol esters

45
Q

What are the sites of cholesterol biosynthesis? (LIAc)

A 
the liver (most common)
intestine 
adrenal cortex
46
Q

What are the stages of cholesterol biosynthesis?

A

acetyl-CoA (C2) -> HMG-CoA (+ HMG-CoA Reductase enzyme) = mevalonate (c6)
mevonate (6) < squalene (30) < cholesterol (27)

47
Q

What is the rate determining step of cholesterol biosynthesis?

A

HMG-CoA (+ HMG-CoA Reductase enzyme) = mevalonate (c6)

48
Q

How is cholesterol biosynthesis controlled?

A

by the amounts of pre-existing cholesterol in the cell
lots of chol = inhibition
insufficient = increased

49
Q

What substance is the target site for statin drugs?

A

HMG-CoA Reductase enzyme

50
Q

How are short-chain FAs transported in the blood?

A

they are bound to blood proteins like albumin

51
Q

How are neutral lipids transported in the blood and why?

A

via lipoproteins - neutral lipids are insoluble in water bc they’re hydrophobic

52
Q

What is the structure of lipoproteins?

A

Neutral lipids carried in a central core

Outer layer of amphipathic PPLPDs and cholesterol

53
Q

What are the four major classes of lipoproteins? (HIV Lilac)

A

HDL, IDL, VLDL

LDL - carries the most cholesterol

54
Q

What is the 2nd most important apoprotein other than LDL?

55
Q

Which apoprotein does LDL contain?

56
Q

What is the relationship with VLDL, IDL and LDL?

A

VLDL unloads triacylglycerols at the tissues
as it loses lipid from these mlcs, becomes IDL
same happens to IDL, which becomes LDL

57
Q

Which is the biggest lipoprotein type?

A

chylomicrons

58
Q

What is the function of chylomicrons?

A

delivers dietary triacylglycerols from the SI to muscle

delivers cholesterol from the liver to the adipose tissue

59
Q

What substances does VLDL transport?

A

endogenously produced triaclyglycerides

cholesterol (from the liver to the tissues)

60
Q

What substances does HDL transport?

A

cholesterol (from tissues to the liver - moving it from tissues)

61
Q

What happens to chylomicron remnants?

A

they’re taken up by the liver and are recycled into VLDL particles - they’re again used to transport TGC and dietary cholesterol to the tissues

62
Q

What happens to the VLDL transportation particles once released from the liver?

A

as they unload, they become LDL, then etc etc

63
Q

What is the role of tissue bound lipases?

A

to digest VLDL particles, allowing the lipids to be released at the cells

64
Q

What identifying features do LDL particles have for their receptors?

A

ApoB particle

65
Q

What happens once LDL particles are taken into the cell?

A

can be stored in the cell as an ester

can be used to make membrane or other biological molecules.

66
Q

What is an advantage of cells taking up cholesterol in the form of LDL from the blood?

A

it means that the cell doesn’t have to sort of spend so much energy actually synthesising cholesterol themselves

67
Q

What is the function of SRBEPS?

A

controls the expression of LDL receptors

68
Q

What is the first thing that happens when cholesterol levels are low within the cell?

A

SRBEPS are activated
they increase the expression of the LDL receptors
there will be more receptors on the membrane
results in increased influx of cholesterol into the cell

69
Q

Where does PCSK9 bind to?

A

LDL receptors

70
Q

What does PCSK9 do once the LDL and receptor has been taken into the cell?

A

it targets the LDL receptor for degradation, stopping it from being recycled back into the membrane

71
Q

What is the overall effect of PCSK9?

A

reduces the amount of LDL and cholesterol that’s been taken into the cell

72
Q

What do apolipoproteins form when they bind to lipids?

A

lipoproteins

73
Q

In what fluids do apolipoproteins transport lipids?

A

blood, CSF and lymph

74
Q

G Why is it called beta oxidation?

A

bc the beta carbon of the FA undergoes oxidation to a carbonyl group

75
Q

What are the functions of oxidase enzymes in peroxisomes?

A

detoxification - alcohol, H2O2 and other harmful chemicals

lysis of FAs to produce H2O2

76
Q

How do FAs become activated?

A

by attaching to CoA in the mitochondria or peroxisomes

M103 T3 (21 decks)

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