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BioChem Exam 2 > Metabolism I > Flashcards

Metabolism I Flashcards

1
Q

What are converted to high energy ATPs to provide energy for cells and tissues?

A
  • glucose
  • FA
  • AA
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2
Q

Sources of ATP

A
  • Adenylate kinase
  • Creatine phosphokinase/phosphocreatine (CPK)
  • Anaerobic metabolism
  • Aerobic metabolism
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3
Q

Glycolysis

A

breakdown of 1 molecule of glucose (6C) into 2 molecules of pyruvate (3C)

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4
Q

Where does glycolysis occur?

A

Cytoplasm

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5
Q

How many steps are there in glycolysis?

A

10 steps

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6
Q

Major points in glycolysis

A

glucose –> C6P –> pyruvate –> acetyl CoA

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7
Q

Three enzymes of glycolysis

A
  • hexokinase (HK)
  • PFK
  • PK
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8
Q

Where does pyruvate go after glycolysis

A
  • Lactate (PDH pathway)

- acetyl CoA –> TCA cycle (PDH pathway)

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9
Q

How many stages is glycolysis broken into?

A

3

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10
Q

Where does the formation of acetyl CoA occur?

A

mitochondria

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11
Q

What enzyme is responsible for pyruvate conversion to acetyl CoA?

A

Pyruvate dehydrogenase complex

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12
Q

How many ATP are generated when converting pyruvate into acetyl CoA?

A

2 ATP

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13
Q

Where does the Kreb’s cycle occur?

A

Mitochondria

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14
Q

What does the Kreb’s cycle depend on?

A

availability of substrates and cofactors

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15
Q

How many ATP molecules are produced from glucose by aerobic respiration?

A

36 ATP

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16
Q

What is the net energy of ATP from glycolysis?

A

2 ATP

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17
Q

What is the net energy of ATP from Kreb’s cycle

A

32 ATP

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18
Q

What regulates glycolysis?

A
  • Hexokinase

- Glucokinase

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19
Q

How many isoforms of hexokinase are present?

A

4

I, II, III and IV

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20
Q

What is HK IV called?

A

glucokinase

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21
Q

Where are HK I - III found?

A

in most tissues

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22
Q

HK I - III Km

A

Low Km for glucose relative to its concentration in blood

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23
Q

What is HK I - III inhibited by?

A

Strongly inhibited by G6P

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24
Q

Where is HK IV found?

A

liver and pancreas

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25
Q

HK IV and Km

A

high KM for glucose

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26
Q

HK IV inhibition

A

less sensitive to inhibition by G6P

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27
Q

What is glucokinase regulated by?

A
  • F6P

- fructose

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28
Q

GK inhibitory protein

A
  • GK-RP

- sequesters GK as an inactive complex in nucleus

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29
Q

Where is GK-RP found?

A

nucleus of liver cells

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30
Q

What promotes the binding of GK to GK-RP?

A

F6P

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31
Q

What inhibits GK?

A

F6P

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32
Q

How is F6P inhibition of GK overcome?

A

by large increase in glucose concentration

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33
Q

Fructose and GK

A
  • fruits
  • vegetables
  • high fructose corn syrup
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34
Q

What does fructose get converted to?

A

F1P

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35
Q

What activates GK?

A

F1P

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36
Q

Role of F1P

A
  • promotes hepatic glucose utilization

- partly responsible for adverse effects of fructose consumption (lipogenesis, hypertriglyceridemia etc)

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37
Q

GK as an enzyme

A

inducible

38
Q

What stimulates GK transcription?

A

Insulin

39
Q

What can a mutation in GK lead to?

A

a form of MODY

40
Q

What does PFK1 catalyze?

A

the first committed step in glycolysis

41
Q

What are the negative effectors of PFK1?

A

ATP
Low pH
Citrate

42
Q

What are the positive effectors of PFK1?

A

AMP (cAMP)

F2,6BP

43
Q

What inhibits PFK1?

A

ATP (negative allosteric effector)

44
Q

What promotes PFK1 activity?

A

AMP (positive allosteric effector)

45
Q

What does F1,6 BP’ase catalyze?

A

an irreversible reaction opposite to that catalyzed by PFK1

46
Q

What doe PFK1 and F1-6BP’ase together catalyze?

A

futile cycle

47
Q

What inhibits F1,6 P’ase?

A

AMP

48
Q

What does the inhibition of F1,6 P’ase lead to?

A
  • increased F1, 6BP

- glycolytic flux

49
Q

What is PFK1 regulated by?

A
  • intracellular pH
  • citrate
  • H + ions
50
Q

What is PFK1 not regulated by?

A

Lactic acid (the end product of glycolysis)

51
Q

What do some tissues prefer as fuels instead of glucose?

A

FA and ketone bodies

52
Q

Why do some tissues prefer FA and ketone bodies over glucose?

A

to spare glucose for use by organs which specifically require glucose for energy (brain)

53
Q

What does citrate inhibit?

A

PFK1

- thus glucose utilization

54
Q

Where does citrate accumulate?

A

in cytosol

55
Q

What inhibits glycolysis?

A

Glycogen

Epinephrine

56
Q

What is a positive allosteric effector of PFK1?

A

F2,6P

57
Q

What happens if there if no F2, 6P?

A

glycolysis cannot occur in liver

58
Q

What triggers adenylate cyclase through cAMP?

A

binding of glucagon to its receptor triggers

59
Q

What does adenylate cyclase through cAMP cause?

A

decrease in F2, 6P

60
Q

What does a decrease in F2, 6P lead to?

A
  • reduces PFK1
  • activates F1, 6BPase
  • inhibit glycolysis
61
Q

F1, 6P and glycolysis

A

intermediate via PFK1

62
Q

F2, 6P and glycolysis

A

side product via PFK2

63
Q

What does F2,6BPase oppose?

A

PFK2 bi-functional enzyme - same protein

64
Q

What inactivates kinase?

A

Phosphorylation

65
Q

What activates phosphatase activity?

A

phosphorylation

66
Q

What activates kinase?

A

dephosphorylation

67
Q

What inactivates phosphatase activity?

A

dephosphorylation

68
Q

What regulates glycolysis?

A
  • PK
69
Q

What inhibits PK?

A

physiological concentration of ATP

70
Q

What activates PK?

A

F1, 6BP

71
Q

Is PK active or inactive in the phosphorylated state?

A

inactive

72
Q

Is PK active or inactive in the dephosphorylated state?

A

active

73
Q

What causes a change in activity of PK?

A

covalent modification by PKA

74
Q

What is PK induced by?

A
  • high carbohydrate intake
  • high insulin levels
  • in liver
75
Q

Glycogen synthase

A
  • converts glucose to glycogen
  • insulin promotes glycogen synthesis
  • fed state
76
Q

Glycogen phosphorylase

A
  • breakdown glycogen to glucose
  • glucagon promotes glycogen breakdown
  • fasted state
77
Q

When is glycogen synthase active?

A

fed state

78
Q

When is glycogen phosphorylase active?

A

fasted state

79
Q

Gluconeogenesis

A

formation of new sugar

80
Q

When is gluconeogeneis activated?

A
  • fasting condition

- during exercise

81
Q

What promotes gluconeogenesis?

A

Glucagon to protect against hypoglycemia

82
Q

What does gluconeogenesis provide glucose for?

A

brain
muscles
erythrocytes

83
Q

Where does gluconeogenesis take place?

A
  • mainly in liver

- small extent renal cortex

84
Q

What are the precursors for gluconeogensis?

A
  • pyruvate
  • lactate
  • glycerol
  • certain AA (alanine, aspartate)
85
Q

When is the Cori cycle active?

A

after exercise

86
Q

Cori cycle

A

muscles get glucose from stored glycogen

87
Q

What is glucose converted to in the Cori cycle?

A

lactic acid

88
Q

What happens to the lactic acid in the Cori

A

redirected to liver for gluconeogensis

89
Q

Where is the glucose released in the Cori cycle?

A

into blood

90
Q

Where is glucose taken up in the Cori cycle?

A
  • muscle

- used for energy and stored as glycogen

BioChem Exam 2 (6 decks)

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