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M104 T2 > M104 T2 L10 > Flashcards

M104 T2 L10 Flashcards

1
Q

What is the role of PFK-1?

A

it converts fructose-6-phosphate to fructose-1,6,-bisphosphate

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2
Q

What molecules can be converted into glucose via gluconeogenesis?

A

lactate from glycolysis
amacs from protein breakdown
glycerol from fat metabolism

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3
Q

What sbustance CAN’T be converted into glucose via gluconeogenesis?

A

FAs from fat metabolism

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4
Q

Where does gluconeogenesis primarily occur?

A

in the liver

it also occurs in the kidneys, e.g. starvation

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5
Q

In what condition are the kidneys gluconeogenic?

A

starvation

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6
Q

What are some of the overall requirements for gluconeogensis?

A

carbon skeletons - a source of carbon required to form glucose molecules
a source of E - for the biosynthesis of glucose mlcs

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7
Q

Where does E in the form of ATP come from?

A

it is provided by metabolism of FAs released by lipolysis in adipose tissue

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8
Q

What is the use of amacs as a source of carbon for gluconeogenesis always associated with?

A

increased rates of urea synthesis

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9
Q

What is the structural formula of urea?

A

H2N - C = O - NH2

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10
Q

What is the equation by which toxic ammonia is converted into urea?

A

NH3 + CO2 + 2H2O + 3ATP + aspartate = urea + fumarate + 2ADP + AMP + 2Pi + PPi

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11
Q

What is the by-product fumerate converted into and where?

A

oxaloacetate in the cytoplasm

oxa is the starting point for gluconeogenesis

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12
Q

What is oxaloacetate used for?

A

it is the starting point for gluconeogenesis

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13
Q

What is the role of fructose-1,6,-bisphosphatase?

A

it reverses the action of PFK-1 by dephosphorylating fructose-1,6-bisphosphate back into fructose-6-phosphate

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14
Q

What is the role of glucose-6-phosphatase?

A

it controls the dephosphorylation of glucose-6-phosphate back to glucose so that it can be exported from the cell

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15
Q

What happens when glucose is phosphorylated to glucose-6-phosphate?

A

it is essentially trapped in the cell because this molecule is charged and can’t across cell membranes

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16
Q

What is the enzyme PFK-1 controlled by?

A

E-dependent allosteric regulation by ATP, AMP and H+

allosteric regulation by nutrients

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17
Q

What molecules alosterically regulate PFK-1?

A

ATP, AMP and H+

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18
Q

What is the effect of ATP on the activity of PFK-1?

A

high levels of ATP inhibit PFK-1
bc ATP = lots of E available in the muscle
this prevents glucose being utilised by glycolysis when there’s plenty of ATP available

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19
Q

What can the presence of ATP, AMP and H+ mlcs in the cell be used to indicate?

A

the amount of E available in the cell

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20
Q

What does allosteric regulation involve?

A

the regulation of enzymes by mlcs present in the cell that are there in either greater or or less amounts

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21
Q

When is AMP present in cells?

A

when ATP has been depleted

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22
Q

What are examples of situations where ATP would be depleted?

A

during muscle contraction or anoxia

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23
Q

What substance does AMP activate?

A

PFK-1

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24
Q

What happens when there’s high levels of AMP in a cell?

A

the rate of glycolysis is increased IOT generate more ATP to replace that which has been depleted

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25
Q

When are H+s increased?

A

during anoxia

during anaerobic muscle contraction due to lactic acid production

26
Q

What is the effect of H+ on the activity of PFK-1?

A

it inhibits PFK-1 and so it inhibits glycolysis

bc H+ prevents the cellular pH from falling too low and damaging the cellular machinery

27
Q

What would happen if H+ concentration in a cell increased unregulated?

A

it could eventually cause a pH in the cell that’s too low and would actually damage the proteins in the cell

28
Q

What can the inhibition of glycolysis by H+ ion conc in the heart be overcome by?

A

the high AMP levels in the heart

29
Q

What are the side effects when there are high AMP levels in the heart inhibiting glycolysis?

A

cellular damage
chest pains experienced in heart attacks
angina

30
Q

Why can high AMP levels inhibit glycolysis in the heart?

A

bc the side effects caused are preferable to not having sufficient levels of ATP - the heart muscle can’t stop can’t have a rest in the way that skeletal muscle can

31
Q

Which nutrients allostericaly regulate PFK-1?

A

Fru-6-P, Fru-2,6-BP and citrate

32
Q

What is fructose-6-phosphate generated from?

A

glucose-6-phosphate that has been phosphorylated upon entry into the cell

33
Q

What do high levels of F-6-P or Fru-2,6-BP indicate?

A

high rates of glucose entry or of glycogen breakdown

34
Q

What is the effect of high levels of F-6-P?

A

stimulates glycolysis so that the high levels of fuel for E production or for fat synthesis

35
Q

What is the most potent allosteric activator?

A

Fru-2,6-BP

36
Q

What is the role of Fru-2,6-BP?

A

it activates PFK-1, stimulates glycolysis to allow for E production or for fat synthesis

37
Q

What is the effect of high levels of citrate?

A

it inhibits PFK-1 and therefore inhibit glycolysis

38
Q

What do high levels of citrate indicate?

A

TCA cycle overload (more acetyl CoA than can be oxidised) or FA oxidation
so there is a need to conserve glucose by inhibition of glycolysis - glucose sparing

39
Q

What is an example of a state in which FA oxidation occurs?

A

starvation

40
Q

How is Fru-2,6-BP generated?

A

from F-6-P by the enzyme PFK-2

41
Q

How is F-6-P regenerated from Fru-2,6-BP?

A

when Fru-2,6-BP is dephosphorylated via Fru-2,6-BPase

42
Q

Where are the molecules of PFK1, PFK-2 & F-2,6-BPase found?

A

in all cells

43
Q

Where are the molecules of F-1,6,BPase found?

A

in the liver & kidneys

44
Q

What is Fru-2,6-BP a potent inhibitor of?

A

F-1,6,BPase

45
Q

What is glycolysis inhibited by?

A

Presence of sufficient E (ATP)
FA oxidation (i.e. citrate) indicating the need for glucose ‘sparing’
H+ ions (lots of lactate)

46
Q

What is glycolysis activated by?

A

Low levels of E (AMP)

Lots of glucose or its metabolites

47
Q

Does lots of available glucose always signal the need for glycolysis?

A

yes but not in the liver

48
Q

How does the muscle use glucose and glycogen for E production?

A

by increasing F-2,6-BP and stimulating glycolysis

49
Q

How does the liver use glucose and glycogen for E production?

A

it uses glucose produced via gluconeogenesis and glycogen to maintain blood glucose so that glycolysis is inhibited

50
Q

What is glucose used for in the liver?

A

to maintain blood glucose

51
Q

Why is extra control of F-2,6-BP required in the liver?

A

bc if glycogen is being mobilised to generate glucose or if oxaloacetate is being used to generate new glucose via gluconeogenesis, then actually the liver does not want to essentially use that glucose in glycolysis for its own E requirements
so if glycogen is being mobilised, if new glucose is being synthesised, that glucose is for export to maintain blood glucose and therefore in the liver, glycolysis needs to be inhibited so that this available glucose is not used by the liver

52
Q

What are the two reactions that need to be controlled in the liver?

A

glycolysis needs to be inhibited

gluconeogenesis needs to be stimulated

53
Q

What is different about the enzymes responsible for the conversion of F-6-P into F-2,6-BP in the liver?

A

the two different enzymes PFK-2 and F-2,6-BPase, in the liver, are actually one protein / enzyme with two active sites

54
Q

What are PFK-1 or F-1,6-BPase directly controlled by?

A

by the level of F-2,6-BP (which is affected by the effect of glucagon on the cells)

55
Q

What happens when the liver is under the influence of glucagon?

A

glucagon increases FA beta oxidation and the rates of lipolysis, so there’s an increased rate of FAs entering into the hepatocytes
these undergo b-oxidation, so acetyl-CoA levels in the cell increase, which feeds back on the two enzymes that control pyruvate = inhibitory effect on pyruvate dehydrogenase, so no more pyruvate is converted to acetyl-CoA
but there’s a stimulatory effect on pyruvate carboxylase, so pyruvate is being directed into oxaloacetate, which is a starting point for glucose synthesis via gluconeogenesis

56
Q

How is gluconeogenesis activated in the liver?

A

Increased fatty acid oxidation leads to increase in acetyl CoA – an allosteric activator of pyruvate carboxylase and inhibitor of pyruvate dehydrogenase – so favours gluconeogenesis over glycolysis

57
Q

What is the effect of increased glucagon in the liver?

A

it inhibits PFK-2 activity and stimulates F-2,6-BPase by phosphorylation (via cAMP-dependent protein kinase) resulting in a fall in F-2,6-BP

58
Q

What is the effect of decreased F-2,6-BP levels in the liver?

A

it reduces activation of PFK-1 (inhibits glycolysis) and relieves inhibition of F-1,6-BPase (stimulates gluconeogenesis)

59
Q

What is gluconeogenesis stimulated by in the short term and how?

A

via glucagon and adrenaline by changes in protein phosphorylation or mobilisation of FAs and production of acetyl CoA

60
Q

What is gluconeogenesis stimulated by in the long term?

A

via enzyme induction by glucagon, glucocorticoids and thyroid hormones

61
Q

What is gluconeogenesis inhibited acutely by and how?

A

insulin via dephosphorylation and suppression of lipolysis and in the long term by suppression of gluconeogenic enzymes

M104 T2 (15 decks)

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