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immu3102 > meds2003 ver.ka > Flashcards

meds2003 ver.ka Flashcards

1
Q

How does muscle contraction use ATP

A

actin and myosin interaction

The faster the contraction, the faster the use of ATP

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2
Q

How is muscle using ATP at rest?

A

maintaining ion gradients, sacroplasmic reticulum and calcium

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3
Q

Outline the features of type1-red muscle

A

contracts relatively slowly

many mitochondria good blood supply

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4
Q

outline the features of type 2b white muscle

A

contracts relatively rapidly
few mitochondria
poor blood supply
full of contractile filaments

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5
Q

What limits ATP production

A

The hydrogen/electron carriers are in short supply

the ADP are in short supply

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6
Q

What is an essential feature of the inner mitochondrial membrane to create a proton gradient

A

The inner mitochondrial membrane is impermeable to protons

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7
Q

How is proton pumps controlled?

A

proton gradient.
Moreover, the proton pumps only flow into the matrix if the ATP is being made, which is how it is coupled.

With no proton pumping there is no hydrogen/electron movement down the electron transport chain

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8
Q

Why is there a need for coupling

A

ATP stores are pathetic

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9
Q

Why is Fatty acids a good energy source

A

Fatty acids are very reduced, so they have a large number of hydrogen

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10
Q

How are fatty acids stored

A

They are stored as triglyceride, which makes them very energy dense, hydrophobic and huge stores build up

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11
Q

what tissues could glycogen be used in

A

all tissues

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12
Q

some facts about glycogen stores

A

hydrophilic, lots of water associated
low stores (about 300g)
inefficient; 16kJ/g

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13
Q

some general facts about glycolysis

A 
happens in all tissues
wholly cytosolic
have no requirement for oxygen
it happens very very fast
it is very very inefficient
ATP generation almost irrelevant
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14
Q

What is the most readily available fuel in gentle exercise

A

glucose.

Glucose transporters move to cell surface

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15
Q

What happens hormonally when we engage in gentle exercise

A

A tiny decrease in blood glucose gives big hormonal responses,
insulin down and glucagon up.
We need this level of control to maintain 5mM of glucose for our brains

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16
Q

What is the effect of low insulin and high glucagon

A

It stimulates glycogen breakdown in the liver and a stimulation of fat breakdown in white adipose tissue

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17
Q

Why do we need to engage in glucose recycling

A

because glucose stores are limited. We need to try substitute glucose where we can

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18
Q

What happens several minutes after gentle exercise

A

fatty acids take over from insulin decrease and glucagon increase.

Glucose is still taken into the muscles
and lactate goes to the liver for the resynthesis of glucose for gluconeogenesis

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19
Q

What happens in moderate exercise

A

the rate of fatty acid utilisation increases but the enzymes that catalyse fatty acid oxidation soon reach their maximum capacity

And the inhibition of glucose oxidation is removed to get some energy from glucose
glucose oxidation occurs
less glucose recycling and liver glycogen stores are depleted faster

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20
Q

Where does the glucose come from in moderate exercise

A

the glucose comes from the liver

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21
Q

What happens when we undergo strenuous exercise

A

muscle glycogen is now broken down

and glycolysis is happening

so we are also forming lactate

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22
Q

Why is glycogen important

A

Because once glycogen has run out, only fatty acid oxidation can be used for ATP generation. And we cannot sprint if there is no glycogen

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23
Q

What happens during sprinting

A

We use type IIb muscles

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24
Q

Why can’t we use fatty acids during sprinting

A

type iib muscles have poor oxygen supply and low mitochondria

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25
Q

Why can’t we use blood glucose

A

type iib muscles used

There would be a delay in transporter recruitment and poor fuel supply

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26
Q

What is the glycolysis happening in the muscle

A

glycogen=>g6p=>pyruvate=>lactate

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27
Q

creatine phosphate

A

creatine phosphate is an instant store of ATP,

creatine phosphate+ADP=> ATP+ creatine

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28
Q

What does NAD oxidise

A

oxidises CH2CHOH

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29
Q

What does FAD oxidise

A

it oxidises CH2CH2 to CHCH

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30
Q

how is fatty acid travelling in the blood

A

bound to serum albumin

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31
Q

How is fatty acid bound in the cytoplasm

A

fatty acid binding protein

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32
Q

What traps Fatty acid

A

CoA

FA+CoA=> Fatty acyl CoA with the help of ATP and fatty acyl synthase

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33
Q

What is CoA

A

A large polar molecule with an important thiol group
pantothenic acid and
3’ phosphoadenosine diphosphate

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34
Q

How is fatty acid travelling into the mitochondria

A

fatty acyl CoA too polar, and too large,
so carnitine acyl transferase 1 removes CoA, and carnitine reacts with fatty acid to form fatty acid carnitine.
Fatty acid Carnitine can then react with CoA to form fatty acid CoA with CAT2, and then the carnitine goes back to the cytoplasm

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35
Q

outline what is the first hydrogen/electron stripping step of fatty acid

A

involves FAD to form a c=c double bond

eventually the c=c double bond is hydrated to form an OH group

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36
Q

Second hydrogen/electron stripping step

A

inolves AND

which then forms a C=0 group that is then attacked by CoA

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37
Q

Each time beta oxidation takes place, the fatty acid part loses an…

A

acetate chunk

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38
Q

Where is GLUT1 found

A

in all cells all the time

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39
Q

Where is GLUT4 found

A

in muscle and adipose tissue

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40
Q

Where is GLUT 2 found

A

in liver and pancreas

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41
Q

What happens in early glycolysis

A

glucose 6 phosphate turns into fructose 6 phosphate which is then phosphorylated using ATP with phosphofructokinase to give fructose 1, 6 bisphosphate, which splits off to give two 3 carbon molecules

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42
Q

What happens in the Return phase

A

g3p ix oxidised with NAD, and a phosphate is added, this 2 phosphate molecule is what causes substrate level phosphorylation, when it reacts with ADP

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43
Q

What is the yield of glycolysis

A

2ATP per glucose 2 pyruvate and 2 NADH

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44
Q

What is the substrate of the krebs cycle

A

Acetyl CoA

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45
Q

Where does the krebs cycle take place

A

in the mitochondria

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46
Q

What is the overall strategy of the krebs cycle

A

completely oxidize acetate carbons to CO2
produce lots of NADH, FADH2 and an ATP

regenerate carrier

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47
Q

What happens when we have no proton gradient (uncoupling)

A

No back pressure to stop protons from pumping
No restriction on hydrogen/electron movement down the lectron transport chain to oxygen

Instant regeneration of NAD from NADH
massive fuel oxidation rate
massive oxygen consumption
no ATP synthesis

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48
Q

What is an example of a natural uncoupling

A

UCP1

49
Q

How does UCP1 work

A

basically it’s function is to generate heat
Noradrenaline binds to a beta 3 receptor which stimulates fatty acid release, and opens the proton channel to allow protons to pass through

50
Q

How are the proteins arranged in the electron transport chain for H+ expelling and H+ consuming reactions

A

h+ expelling reactions are on the outside

H+ consuming reactions are on the matrix side

51
Q

approximately how many protons are pumped out for each NADH

A

about 10

52
Q

What are 3 interesting features of NAD

A

it is reoxidised by complex 1
it likes to rip H/e off from CH-OH groups to convert them to C=O groups
it is a dinucleotide-2 nucleotides joined back to back

the nicotanamide group is derived from nicotinic acid

53
Q

FAD 3 interesting features

A

present in complex II
likes to rup H from a saturated hydrogen carbon chain

it is totally stuck in complex II

54
Q

what are 5 interesting features about UQ

A

UQ is very hydrogphobic
they also pick up hydrogens from complex II

reduced UQ is UQH2
UQH@ transfers hydrogens to complex III

55
Q

What is the function of cytochrome C and iron

A

Cytochorme C picks up electrons from complex III and gives the electrons to complex IV

They have a prosthetic group which changes from ferrous to ferric

56
Q

how do you get NADH to the ETC

A

glycerol 3 phosphate shuttle

Malate Aspartate Shuttle

57
Q

What is the quirk of the G3P shuttle

A

it bypasses complex I

58
Q

outline what happens in the Glycerol 3 phosphate shuttle

A

dihydroxyacetone phosphate protonated by NADH and cytoplasmic glycerol 3 phosphate dehydrogenase then goes to glycerol 3 phosphate.

Glycerol 3 phosphate hydrogens protonate E- FAD which creates a cycle

59
Q

malate aspartate shuttle

A

too hard to describe

60
Q

What are the 4 routes to Q

A

from complex 1
from complex 2
from its first step of beta oxidation
from the glycerol 3 p shuttle

61
Q

How does the skunk cabbage uncouple the reactions

A

?

62
Q

What are the dangers of free radicals

A

electrons in the UQ pool can react with molecular oxygen to produce free radicals
and this can cause mutations to DNA

The free radicals then move to complex IIi

63
Q

How is ATP made from 2 ADP

A

with adenylate kinase

translates a small change in ATP to a relative large change in AMp

64
Q

Relative ATP concentration before ATP depletion

A

About 5.0mM

65
Q

relative ATP concentration after ATP depletion

A

4.5mM

66
Q

relative ADP concentration before ATP depletion

A

1.0mM

67
Q

Relative ADP concentration after ATP depletion

A

1.0mM

68
Q

Relative AMP concentration before ATP depletion

A

0.1mM

69
Q

Relative AMP concentration after ATP depletion

A

0.6mM

70
Q

properties of the rate limiting step

A

irreversible

1) need alternative enzymes to go back
2) not equilibrium under physiological conditions
3) committed steps

Saturated with substrate

1) low Km or [S]»Km
2) working at Vmax

71
Q

What are the 3 main ways to change the rate/flux of the metabolic pathways

A

1) make the rate limiting enzyme go faster/slower
2) turn the rate limiting enzyme on/off or make it work the other way
3) increase the rate of transcription/translation of the rate limiting step or change its rate of degradation

72
Q

Give an example of allostery in the regulation of the metabolic pathway

A

PFK,
it does not like a high concentration of its substrate ATP.

it has binding sites for AMP away from the active site

Binding AMP changes the way that PFK responds to ATP

PFK also binds citrate allosterically
Citrate inhibits PF when citrate concentrations are high.

73
Q

Give an example of feedback inhibition in the regulation of the metabolic pathway

A

The initial glucose trapping reaction.
Hexokinase
Inhibition by the product G6P prevents excessive trapping, so if G6P is not used, glucose is not trapped.

74
Q

Give an example of covalent modification in the regulation of the metabolic pathway

A

PDH
PDH kinase, PDH phosphatase,
acetyl CoA
insulin

75
Q

amphiphilic molecules can act as

A

detergents to emulsify fat into tiny particles/ micelles

76
Q

What are bile salts made from

A

made from cholesterol in the liver.

It is the addition of polar groups

77
Q

Where is Bile Salts secreted and stored

A

stored in the gall bladder, and released towards the small intestine

78
Q

What happens to bile after the digestion of fat

A

It is reabsorbed and taken back into the liver via the hepatic portal vein

79
Q

Why is the production of bile salts important from a metabolism standpoint

A

production of bile salts is the only way in which cholesterol is metabolised and disposed

80
Q

how are fat contained

A

fat is contained in the core of micelles formed by bile salts.
Chyme, emulsion, and easy for lipase to interact with

81
Q

What is the function of pancreatic lipase

A

it hydrolyses fat into fatty acid and glycerol plus a mixture of mono and diacyl glycerols

82
Q

Where are pancreatic lipase found

A

everywhere

83
Q

What is the function of apoproteins

A

They act as enzymes and help with docking

84
Q

Where are chylomicrons made

A

in the intestinal cells from the gut, and released into the lymphatic system

85
Q

packaging of cholesterol

A

Where exactly does this fit. Cholesterol is transformed into cholesteryl ester from acyl coa cholesterol acyl transferase.

This forms the core of a lipoprotein.

86
Q

What do chylomicrons do?

A

They interact with lipoprotein lipase (LPL) on the surface of cells and capillaries

The fat is hydrolysed into fatty acids and glycerol, and then taken up for storage or oxidation.

Apparently you could re-esterfy it with glycerol 3 phosphate

87
Q

What happens with the chylomicrons as it passes through the capillary

A

Fat is removed from chylomicrons

88
Q

What happens to chylomicrons in the end

A

They get endocytosed in the liver. There is still quite a bit of fat remaining in the liver

89
Q

What is the liver’s function in fat import and export

A

The liver assembles very low density lipoproteins from fat and cholesterol esters

The fat could also be made by lipogenesis. The VLDL is then excreted into the blood stream.

90
Q

What happens when VLDL is in the blood

A

LPL in the peripheral tissues works in peripheral tissues on VLDL, depleting the fat and creating low density lipoprotein

91
Q

What is the function of LDL

A

Tissues take up LDL through the LDL receptor

This is how cholesterol is delivered to the tissues

92
Q

How do cells create their own cholesterol

A

HMG-CoA reductase basically turns acetate into choletserol.

93
Q

What is HMG-CoA reductase regulated by

A

It is regulated by insulin, cholesterol levels, gene expression, enzyme degradation and even a circadian rhythm

94
Q

Why is elevated blood LDL bad

A

LDL particles become oxidised with time.
Macrophages take up ox-LDL without control-becoming foam cells

This creates an inflammatory environment that encourages the formation of plaques

95
Q

What is the function of HDL

A

They basically get a cargo of cholesterol, and then bring it to the liver. It happens when the cells want to get rid of cholesterol.

96
Q

What does CETP do

A

They catalyse the exchange of cholesterol ester for triglyceride.
They could apparently interact with a VLDL or a chylomicron when doing this

97
Q

What are the consequences of having CETP

A

HDL takes back more fat and less cholesterol

Cholesterol remains in circulation

VLDL enriched with cholesterol

98
Q

What are functions of insulin

A

Insulin stimulates glucose uptake in the GLUT-4s in the muscle and adipose tissue and the conversion to storage products.

Therefore it can cause increased oxidation

99
Q

Difference between intolerant and diabetic

A

Intolerant has normal fasting glucose, but sluggish clearance.
Diabetic has fasting hyperglycemia. Relentless exposure to high concentration of glucose

100
Q

What are consequences of amylose being a linear structure

A

it can form helices that are difficult for amylases to penetrate. And because it is difficult to penetrate, there is sometimes flatulence, because the amylose has stayed in the body too long.

101
Q

What does the glycemic index describe?

A

The post prandial glucose response.

102
Q

What is the test food and reference food

A

Reference food is normally 50 g glucose

the test food is usually an amount that will give 50 g of digestible carbohydrate.

103
Q

What is the average GI of modern grains

A

over 80

104
Q

What is the average GI of legumes

A

under 30.

105
Q

What time periods matter when thinking about GI

A

over 1 hr 30 minutes is what matters

106
Q

Should GI apply to non starches?

A

Sugary foods or low GI because half the carbohydrates are fructose. Similarly, fructose containing foods are low GI

Somtimes galactose is used in our dairy food

107
Q

Outline how glycogen is synthesised

A

glucose 6 phosphate is turned into glucose 1 phosphate and then glucose 1 phosphate is turned into UDP glucose after using UTP to release PP. The UDP glucose then reacts with glycogen and basically elongates the glycogen. The synthesis is from C1 through to C4

108
Q

How does glycogen synthase work?

A

Basically UDP glucose has its UDP removed, and then the 1’ carbon forms a glycolytic bond between 1’ and 4’

109
Q

What enzyme causes branching?

A

Glycogen branching enzyme

110
Q

What is glycogen synthase regulated by

A

It is regulated by reversible phosphorylation

It is active when dephosphorylated

111
Q

What enzyme does insulin stimulate which also has an effect on glycogen synthase

A

insulin could stimulate protein phosphatase 1, also known as PPI. This causes GS to be dephosphorylated and active, so Insulin could activate GS

112
Q

What is the function of phosphofructokinase

A

It is the rate limiting step of glycolysis

113
Q

So what is phosphofructokinase regulated by

A

it is regulated allosterically by AMP, and low energy charge

114
Q

how does insulin indirectly activate PFK

A

insulin stimulates GS, Glycogenesis is anabolic, and therefore requires ATP. This drops and increases ADP and AMP. PFK is regulated allosterically by AMP and therefore this signals to store fuels to be burnt

115
Q

Glucokinase properties

A

rapidly converts glucose to G6P. It is not inhibited by the build up of G6P. High Km for glucose is not saturated by high levels of liver glucose so G6P rapidly increases as blood glucose rises

116
Q

What is the effect of G6P on inactive glycogen synthase

A

it could phosphorylate GS and it also stimulates the dephosphorylation of GS

117
Q

What is the difference between glycogenolysis in the liver and in the muscle

A

in the liver, there is a “push” mechanism where glycogenesis responds to blood glucose without the need of insulin. Although insulin will stimulate glycogen synthase further

In muscle G6P never gets high enough to stimulate GS.
The push method does not happen in muscle
It is more of a pull as insulin stimulates GS and drags glucose into glycogen

118
Q

what is the difference between glucokinase and hexokinase?

A

glucokinase only works on glucose, it has a high Km for glucose
It is not inhibited by G6P
only presents in liver, beta cells
responsive to changes in glucose blood

Hexokinase works on any 6C sugar, low as fuck Km. It is strongly inhibited by its product G6p. Present in all tissues. Easily saturated.

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