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Metabolism > Integration of metabolism > Flashcards

Integration of metabolism Flashcards

1
Q

What can the brain not use as a metabolic fuel source

A

fatty acids

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2
Q

where is the body’s main carb store

A

liver

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3
Q

what is glucose stored as

A

glycogen

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4
Q

what method of respiration does skeletal muscle do in light contraction

A

ox phos

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5
Q

why can’t skeletal muscle do ox phos in vigorous exercise

A

ATP consummation faster than supplied, limited by O2 and glucose/fatty acid

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6
Q

what does muscle do in vigorous exercise

A

break down glycogen

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7
Q

what happens in anaerobic respiration

A

pyruvate to lactate which enters liver

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8
Q

What fuel can the brain use

A

ketone bodies and glucose

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9
Q

hypoglycaemia causes…

A

fainting and coma

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10
Q

hyperglycaemia causes..

A

irreversible change

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11
Q

How is heart designed for aerobic respiration

A

many mt

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12
Q

what fuel does the heart use

A

TCA substrates: fatty acid and ketone bodies

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13
Q

loss of O2 to heart causes

A

MI

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14
Q

metabolic processes that take place in liver

A

glycolysis, gluconeogenesis, transamination, lipoprotein metabolism

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15
Q

how much of body’s metabolic rate does liver do

A

20%

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16
Q

what happens to excess glucose - 6- phosphate

A

turns to glycogen - liver and muscle

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17
Q

what happens to aexcees acetyl CoA

A

turns to fatty acid

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18
Q

in fasting what happens to acetyl CoA

A

ketone body production

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19
Q

how can pyruvate and TCA intermediates make AA

A

backbones form nucleotides

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20
Q

how does glucose-6-phosphate contribute to the production of NADPH

A

make nucleotides via pentose phosphate pathway

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21
Q

at what glucose conc will the body become hypoglycaemic

A

3mM

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22
Q

How does the body avoid hypoglycaemia

A

breakdown glycogen, release fatty acids, convert acetyl CoA to ketone bodies

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23
Q

how long does it take for glycogen stores to be depleted

A

12-18 hours

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24
Q

purpose of gluconeogenesis

A

produce glucose from non-carb sources (pyruvate)

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25
Q

when is gluconeogenesis important

A

starvation

26
Q

why is gluconeogenesis not a reversal of glycolysis

A

different enzymes - irreversible reactions

27
Q

where does gluconeogenesis occur

A

liver

28
Q

what does gluconeogenesis need and why

A

ATP source, make reactions energetically favourable

29
Q

which precursors enter gluconeogenesis

A

lactate, aa, glycerol

30
Q

How can lactate regenerate pyruvate

A

Cori cycle - LDH

31
Q

Where do AA come from for gluconeogenesis

A

diet/breakdown of muscle

32
Q

What does triglyceride hydrolysis do?

A

yield fatty acid and glycerol - glycerol backbone generate DHAP

33
Q

which enzymes catalyse the irreversible reactions in glycolysis

A

hexokinase, phosphofructokinase, pyruvate kinase

34
Q

enzymes in gluconeogenesis

A 
pyruvate carboxylase (p - oxyloacetate) 
phospoenolpyruvate carboxykinase (o-phospoenolpyruvate) 
Fructose 1,6 bisphosphatase(fructose 1,6 bp - f 6 p)

glucose 6 phophotase (g-6-p - glucose)

35
Q

where does pyruvate decarboxylase act

A

mt

36
Q

waste product of deamination

A

urea

37
Q

What are the glycogenic AA skeletons

A

Pyruvate, alpha - ketoglutarate, succinyl CoA, fumarate, oxaloacetate

38
Q

what are the ketogenic aa skeletons

A

acetyl CoA, acetoacetyl CoA

39
Q

What are glucogenic AA

A

skeleton give ris to glucose by gluconeogenesis

40
Q

what are ketogenic AA

A

used to synthesis fatty acid and ketone bodies

41
Q

How is the increased demand for glucose met?

A

increase in the number of glucose transporters on membrane of muscle cells

42
Q

what does adrenaline do

A

increase glycolysis and gluconeogenesis rate, increase release of fatty acids

43
Q

why is pyruvate converted to lactate in anaerobic respiration

A

restore NAD+ levels

44
Q

Which reactions are the best to control to control metabolic pathways

A

irreversible steps

45
Q

How can you control metabolic pathways

A

product inhibition, signalling molecules

46
Q

Km hexokinase 1 (muscle)

A

o.1mM

47
Q

effect of low Km

A

active at low glucose conc

48
Q

What inhibits hexokinase 1

A

glucose-6-phosphate

49
Q

Km of hexokinase 1V (liver)

A

4mM

50
Q

effect of high Km

A

less sensitive to blood glucose conc

51
Q

sensitivity of hexokinase 1V to glucose-6-phosphate

A

low

52
Q

where is glucose-6-phosphotase found

A

liver

53
Q

What do glucocorticoids do

A

increase synthesis of met enzymes concerned with glucose availability

54
Q

where are adrenaline and glucocorticoids secreted from

A

adrenal glands

55
Q

insulin effects:

A

increased glucose uptake, liver and muscle, triglyceride synthesis, increased use of metabolic intermediates (stimulatory effect on synthesis and growth)

56
Q

to stop glucose levels dropping…

A

glucagon secreted, gluconeogenesis, fatty acid breakdown as a substrate for ATP production.

57
Q

what happens after prolonged fasting

A 
glucagon/insulin  ratio increases
hydolysise fatty acids 
TCA intemediates break down 
protein break down 
ketone bodies from fatty acids and aa
58
Q

overall effect of diabetes

A

metabolism controlled as if in starvation

59
Q

what causes acidosis

A

increase in ketone bodies

60
Q

How does diabetes cause cardiovascular problems

A

increased fatty acids and lipoprotein levels

61
Q

effect of glucagon

A

stimulate gluconeogenesis

62
Q

risk of relative excess of glucagon compared to insulin

A

high heptic output of glucose - hyperglycaemia

Metabolism (12 decks)

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