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module 104 - theme 2 > regulation of carbohydrate metabolism > Flashcards

regulation of carbohydrate metabolism Flashcards

1
Q

where does glycolysis occur?

A

in all tissues

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2
Q

what is glycolysis important?

A

energy in the brain and red blood cells and also for contracting skeletal muscle

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3
Q

what percentage of the body’s total usage of glucose is by red blood cells?

A

10%

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4
Q

what are the 3 examples of de novo glucose synthesis from non-carbohydrate precursors?

A

1) lactate from glycolysis
2) amino acids from protein breakdown
3) glycerol (but NOT fatty acids) from fat metabolism

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5
Q

where does gluconeogenesis?

A

liver and the kidney

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6
Q

what does gluconeogenesis do?

A

maintains blood glucose during fasting, starvation or when glycogen reserves are depleted to preserve glucose-dependent cerebral function and red blood cell metabolism

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7
Q

why isn’t gluconeogenesis just the reverse of glycolysis?

A

it has a unique set of enzymes to overcome energetically unfavourable reactions and introduce points of control

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8
Q

what are the requirements for gluconeogenesis?

A

1) a source of carbon for formation of glucose molecules

2) a source of energy for biosynthesis

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9
Q

where do you get the source of carbon for gluconeogenesis?

A

it is provided for lactate, amino acids or glycerol released from TGs by lipolysis in adipose tissue

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10
Q

where do you get the source of energy for gluconeogenesis?

A

provided by metabolism of fatty acids released by lipolysis in adipose tissue

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11
Q

what must happen first for amino acids to be used in glucose production?

A

it must first be transaminated to lose their ammonia

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12
Q

why must ammonia be eliminated from the body?

A

it is toxic to cells

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13
Q

what happens to ammonia so it isn’t toxic to the cells?

A

it is converted to urea in the liver and then passed out into the bloodstream and extremed by the kidney

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14
Q

what is the equation for the conversion of ammonia to urea?

A

NH3 + CO2 + 2H2O + 3ATP + aspartate —> urea + fumarate

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15
Q

what is fumarate converted to?

A

oxaloacetate

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16
Q

what overcomes the irreversible steps in glycolysis?

A

expression of gluconeogenetic enzymes

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17
Q

what are the 3 stages of glycolysis?

A

1) glucose
2) glucose broken down
3) pruvate

18
Q

what are the 3 stages of gluconeogenesis?

A

1) oxaloacetate (pyruvate)
2) glucose formed
3) glucose

19
Q

what allosterically regulates PFK-1?

A
  • ATP
  • AMP
  • H+
20
Q

what affect does ATP inhibition have on the regulation of glycolysis?

A
  • sign of high energy levels in muscle
  • prevents glucose being utilised by glycolysis when ATP is available
  • co-ordinates glycolysis with glycogen breakdown via phosphorylase
21
Q

what role does AMP have on the regulation of glycolysis?

A
  • leads to activation
  • competes with ATP
  • increases glycolysis and energy production
  • co-ordinates glycolysis and glycogen breakdown via phosphorylase
22
Q

how is PFK-1 regulated by H+?

A
  • H+ increased during anoxia or anaerobic muscle contraction as a result of lactic acid production
  • inhibits glycolysis to prevent cellular pH falling too low and damaging the cellular machinery
  • in heart it can be overcome by high AMP in cellular damage and chest pains experienced in heart attacks and angina
23
Q

how is PFK-1 regulated by nutrients?

A
  • PFK-1 is also subject to regulation by Fru-6-P, Fru-2,6-BP and citrate
  • Fru-6-P activates which is a sign of high rates of glucose entry or glycogen breakdown. stimulates glycolysis to allow utilisation for energy production or fat synthesis
  • Fru-2,6-BP is also a signal of high rates of glucose entry or glycogen breakdown and leads to activation. stimulates glycolysis to allow utilisation for energy production or fat syntheis
  • citrate inhibits which signals TCA cycle overload or fatty acids oxidation and the need to conserve glucose by inhibition of glycolysis
24
Q

what is the most potent allosteric activator known?

A

Fru-2,6-BP

25
Q

what synthesises Fructose-2,6-biphosphate?

A

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

26
Q

what is the most potent allosteric activator of PFK-1?

A

fructose-2,6-biphosphate

27
Q

what does fructose-2,6-biphosphate do?

A

it isn’t involved in metabolic pathways - it acts solely to reinforce allosteric control on PFK-1

28
Q

what is the energy status of ATP with the regulation of glucose at PFK-1?

A
  • signal of maximum energy status

- keeps PFK-1 inhibited in the resting cell to conserve glucose

29
Q

what is the energy status of AMP with the regulation of glucose at PFK-1?

A
  • signal of reduced energy status
  • stimulates glycolysis to increase cellular levels of ATP
  • ensures that glycogenolysis and glycolysis are coordinated
30
Q

what is the energy status of H+ ions with the regulation of glucose at PFK-1?

A
  • raised during anoxia by lactic acid
  • inhibits glycolysis to prevent cell pH falling and damaging cellular machinery
  • can be overcome by AMP (heart)
31
Q

what is the role of F-6-P in the nutrient regulation of glucose at PFK-1?

A
  • signals glucose entry or glycogen breakdown

- stimulates PFK-1 and glycolysis for energy and fat synthesis

32
Q

what is the role of F-2,6-P2 in the nutrient regulation of glucose at PFK-1?

A
  • signals glucose entry or glycogen breakdown

- stimulates PFK-1 and glycolysis for energy and fat synthesis

33
Q

what is the role of citrate in the nutrient regulation of glucose at PFK-1?

A
  • signals TCA cycle overload or fatty acid oxidation

- need to inhibit glycolysis and conserve glucose

34
Q

what is glycolysis inhibited by?

A
  • presence of sufficient energy
  • fatty acid oxidation indicating the need for glucose ‘sparing’
  • H+ ions
35
Q

what is glycolysis activated by?

A
  • low levels or energy

- lots of glucose or its metabolites

36
Q

what does the muscle use glucose and glycogen for?

A

energy production by increasing F-2,6-Bp and stimulating glycolysis

37
Q

what does the liver use glucose produced via glujconeogeneis and glycogen for?

A

maintain blood glucose so glycolysis is inhibited

38
Q

what is the role of fructose-2,6-biphosphate in the liver?

A
  • PFK-2 and F-2,6-BPase are a single tandem enzyme with 2 active sites
  • phosphorylation inhibits PFK-2 and stimulates F-2,6-BPase = decrease F-2,6-BP
  • neither PFK-1 nor F-1,6-BPase are directly controlled by hormones through phosphorylation but by level of F-2,6-BP which is affected by hormones
39
Q

what happens with the activation of gluconeogenesis?

A
  • increased fatty acid oxidation leads to increase in acetyl CoA: an allosteric activator of pyruvate carboxylase and inhibitor of pyruvate dehydrogenase, so favours glujconeogeneis over glycolysis
  • increased glucagon inhibits PFK-1 activity and stimulates F-2,6-BPase by phosphorylation resulting in a fall in F-2,6-BP
  • decreased F-2,6-BP levels reduce activation of PFK-1 and receives inhibition of F-1,6-BPase
40
Q

how is gluconeogenesis regulated by hormones?

A

stimulated in the short term by glucagon and adrenaline by changes in protein phosphorylation or mobilisation of fatty acids and production of acetyl CoA

41
Q

how is gluconeogenesis hormonally regulated in the long term?

A

stimulation occurs through enzyme induction by glucagon, glucocorticoids and thyroid hormones

42
Q

what acutely inhibits hormonal regulation of gluconeogenesis?

A

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

module 104 - theme 2 (18 decks)

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