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GI > Metabolism Revision > Flashcards

Metabolism Revision Flashcards

1
Q

where does fatty acid synthesis occur

A

in the cytoplasm

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2
Q

what breaks down triglycerides into fatty acids and glycerol

A

via lipolysis (lipases)

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3
Q

what acitvates fatty acids

A

the addition of a CoA group= makes fatty acyl-CoA

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4
Q

what then happens to acetyl CoA

A

is a two carbon precursor for entry into the krebs cycle

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5
Q

what does carnitine allow

A

transport of fatty acyl into mitochondrian as fatty acyl-carnitine

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6
Q

what is the main storage form of lipids in the body

A

triglycerides

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7
Q

what do some lipids contain

A

phosphate groups, carbohydrates, proteins

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8
Q

can fatty acids be used for gluconeogenesis

A

no

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9
Q

are lipids mostly hydrocarbon and water insoluble or soluble

A

yes hydrocarbon

mostly water insoluble

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10
Q

lipid absorption is required for the absorption of some what

A

vitamins

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11
Q

what is the first step of fat catabolism

A

lipolysis

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12
Q

do fatty acids have to be activated for fat catabolism

A

no

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13
Q

where does activation of fatty acids occur

A

in the cytoplasm

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14
Q

what is the pathway for breakdown of fatty acids called

A

beta oxidation

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15
Q

where does beta oxidation occur

A

in the mitochondrian

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16
Q

what are the products made from each beta oxidation cycle

A

1 acetyle-CoA, 1 FADH2, 1 NADH + H+, 1 fatty acyl-CoA (which has been shortened by 2 carbon atoms)

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17
Q

how many rounds of beta oxidation occur for an even numbered saturated fat

A

if fat= C2n, number of oxidation cycles= n-1

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18
Q

how many rounds of beta oxidation will a C16 fat undergo

A

C16= C2n=16 carbons

16/2 -1 = 7 oxidation cycles

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19
Q

what will the products be for the breakdown of a C14 fatty acid

A

7 acetyl-CoA, 6 NADH + H+, 6 FADH2

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20
Q

when and where are ketone bodies formed

A

formed in the liver under fasting conditions

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21
Q

what are ketone bodies formed from

A

acetyl-CoA from beta oxidation

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22
Q

what is the role of ketone bodies

A

diffuse into blood stream and travel to peripheral tissues where they are important molecules of energy metabolism in the brain, heart muscle and renal cortex

important in energy production (TCA cycle) and neurotransmitter synthesis

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23
Q

what happens when ketone bodies are metabolised

A

converted back to acetyl-CoA which then enters the TCA cycle

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24
Q

what is the TCA cycle

A

stored energy is released through the oxidation of acetyl CoA

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25
Q

what symptom is seen when the body produces acetone

A

expired fruity breath

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26
Q

when do ketone bodies accumulate

A

in extreme starvation as a by product of beta oxidation

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27
Q

what can ketone bodies cause

A

ketoacidosis

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28
Q

where does fatty acid synthesis main occur (organ)

A

in the liver

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29
Q

what does the process of fatty acid synthesis drive

A

the process of lipogenesis (formation of fat)

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30
Q

what is used to generate acetyle CoA

A

glucose

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31
Q

what does the enzyme acetyl-CoA carboxylase do

A

converts acetyle CoA to malonyl CoA

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32
Q

what is malonyl CoA

A

the major fatty acid synthesis precursor

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33
Q

what regulates acetyl CoA activity

A

nutrient and energy status

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34
Q

where does degeneration of fatty acid occur

A

in the mictochondrian matrix

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35
Q

what reductant does fatty acid synthesis require

A

NADPH

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36
Q

what oxidant does fatty acid degredation require

A

NAD+, FAD

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37
Q

what is the maximum length of fatty acid made

A

C16

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38
Q

what increases the rate of acetyl CoA carboxylase (and therefore the rate of conversion of acetyl CoA to malonyl CoA)

A

citrate, insulin

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39
Q

what decreases the rate of acetyl CoA carboxylase (and therefore the rate of conversion of acetyl CoA to malonyl CoA)

A

palnitoyl CoA, AMP, glucagon, epinephrine

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40
Q

how does insulin regulate acetyl- CoA carboxylase

A

signals the fed state- stimulates the storage of fuels and synthesis of proteins

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41
Q

how do glucagon and epinephrine regulate acetyl CoA carboxylase

A

glucagon signals the staved state

epinephrine signals the requirement for energy

both mobilise glucagon stores

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42
Q

how does citrate regulate acetyl CoA carboxylase

A

stimulates allosterically- citrate levels are high when acetyl CoA and ATP are abundant

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43
Q

how does palmitoyl CoA regulate acetyle CoA carboxylase

A

is abundant when fatty acids are in excess

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44
Q

is fatty acid synthesis an oxidative or reductive process

A

reductive

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45
Q

what transports acetyl groups from the mitochondrian to the cytoplasm

A

citrate

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46
Q

does fatty acid synthesis require NADPH

A

yes

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47
Q

the donor molecule of carbon atoms to a growing fatty acid is

A

malonyl CoA

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48
Q

what does a lot of citrate stimulate

A

acetyl CoA carboxylase

49
Q

what effect does the binding of citrate to acetyl CoA have

A

activates the catalytic effect of the enzyme

50
Q

where is urea synthesised

A

in the liver

51
Q

where does the nitrogen in urea come form

A

one from free ammonium, other from aspartic acid

52
Q

where is the carbon in urea from

A

CO2

53
Q

what happens to the amino group of the amino acids in the formation of urea

A

is removed

54
Q

does removal of amino acid groups in urea formation only occur in the liver

A

no

55
Q

can carbon skeletons of all amino acids enter the TCA cycle

A

yes

56
Q

can glucogenic amino acids be used to form glucose

A

yes

57
Q

can ketogenic amino acids be completely oxidised in the TCA cycle

A

yes

58
Q

is free ammonium toxic

A

yes

59
Q

what is the rate limiting step of glycogen breakdown

A

when glycogen phosporylase turns glycogen into glucose 1 phosphate

60
Q

what are the two possible outcomes of glycogen breakdown

A

glucose formation or glycolysis

61
Q

how does glucose enter the blood

A

GLUT2 transporter

62
Q

where is glucose 6 phosphate turned into glucose

A

only in the liver

63
Q

how does gluconeogensis proceed

A

via the synthesis of oxaloacetate in the mitochondrian

64
Q

is gluconeogenesis energy consuming

A

yes

65
Q

what is glycogenin and what is its role

A

a protein that sits at the centre of a glycogen polymer

has a catalytic activity, can covalently bind up to 4 glucose molecules to itself, essential in the formation of a glycogen polymer

66
Q

what can glycogen synthase only add glucose residues to

A

an existing glycogen chain

67
Q

where are amino acids oxidised

A

in the TCA cycle

68
Q

what are amino acids pre cursors for

A

gluconeogenesis

69
Q

can liver glycogen serve as a source for blood glucose

A

yes

70
Q

can muscle glycogen be used for energy generation outside of the muscle cell

A

no

71
Q

what must glucose be bound to before it can be transferred into glycogen

A

UDP

72
Q

can glycogen synthase introduce new branches

A

no

73
Q

can liver cells create free glucose from glycogen

A

yes

74
Q

does glucagon inhibits glycogen synthesis and stimulate glycogen breakdown

A

yes

75
Q

does insulin inhibit glycogen breakdown and stimulate glycogen synthesis

A

yes

76
Q

is gluconeogensis a pathway for the synthesis of new glucose from non carbohydrate precursors

A

yes

77
Q

true or false: lactate, glycerol and glucogenic amino acids are precursors for gluconeogensis

A

true

78
Q

true or false: gluconeogensis is glycolysis run in reverse

A

false

79
Q

does gluconeogenesis mainly occur in the liver

A

yes

80
Q

is gluconeogenesis energy consuming

A

yes

81
Q

does glucagon inhibit gluconeogensis

A

no it stimulates it

82
Q

does insulin inhibit gluconeogenesis

A

yes

83
Q

what do catabolic pathways do

A

break down substances for energy generation- uses reduced fuel to make oxidised products

84
Q

what do anabolic pathways do

A

synthesise complex molecules out of smaller ones in energy-consuming reaction- uses oxidised precursors to make reduced biosynthetic products

85
Q

what do anabolic pathways require

A

ATP for energy, reducing force in the from of NADPH

86
Q

what do catabolic pathways generate

A

reduced cofactors which can drive oxidative phosphorylation

87
Q

how many ATP does glycolysis produce per glucose thats broken down

A

2

88
Q

what forms the first stage of carbohydrate catabolism

A

glycolysis

89
Q

where does glycolysis occur

A

cytoplasm

90
Q

how much NADH + H+ does glycolysis produce per glucose molecule

A

2

91
Q

what are the three stages of glycolysis

A

1- glucose is trapped and destabilised

2- two interconvertible three carbon molecules

3- ATP generated

92
Q

can pyruvate directly enter oxidative phosphorylation

A

no

93
Q

what is pyruvate converted into that enters the TCA cycle

A

acetyl CoA

94
Q

what does the TCA cycle provide precursors for

A

gluconeogenesis

95
Q

breakdown products from what feed into the TCA cycle

A

carbohydrate, fat and protein metabolism

96
Q

does the TCA cycle consume NADH and FADH2

A

no

97
Q

where does the TCA cycle hapoen

A

in the mitochondrial matrix

98
Q

briefly describe the TCA cycle

A

A two-carbon unit (from acetyl-CoA) condenses with a four-carbon unit

The resulting six-carbon unit is decarboxylated twice
-yields CO2

Four oxidation reactions
-yield NADH + H+ and FADH2

One GTP is formed
-energy

The four-carbon unit is recreated (to make the 6 carbon unit)

99
Q

in oxidative phosphorylation what happens to NADH and FADH2

A

are tranferred onto oxygen

100
Q

where is the electron transport chain located

A

in the inner mitochondria membrane

101
Q

in oxidative phosphorylation where are protons pumped from and to

A

from mitochondrian matrix to intermembrane space

102
Q

what direction is the proton conc gradient

A

from intermembrane space to mitochondrial matrix

103
Q

what is proton flow coupled to

A

ATP synthesis

104
Q

what systems does oxidative phosphorylation consist of

A

two separate proton pump systems

105
Q

in oxidative phosphorylation what are electrons from NADH and FADH2 used to do

A

reduce O2 to H2O

106
Q

energy from what pumps protons

A

electrons from NADH and FADH2

107
Q

what does NADH donate electrons to

A

complex I

108
Q

what does FADH2 donate electrons to

A

complex II

109
Q

what complexes transport electrons alongside the pumping of H+

A

I, III and IV

110
Q

what is the P/O ratio

A

a measure of the number of ATP molecules formed per oxygen atom reduced

111
Q

what is the redox potential of a reduced molecule

A

its likelihood to loose an electron (in comparison with H2)

112
Q

what does a more negative redox potential mean

A

it is more likely to loose an electron

113
Q

how is the transfer of electrons linked to redox potential

A

Electrons can be transferred from molecules with negative redox potentials to those with more positive redox potentials

114
Q

what does the difference in redox potential between substrate and product of a redox reaction relate to

A

the free energy change of the reaction

115
Q

does NADH have a more positive or nagative redox potential than FADH2

A

more positive

116
Q

what does a negative redox redox potential mean

A

the reduced form has a lower affinity for electrons that H2

117
Q

what does a low redox potential mean (e.g. in oxygen)

A

that it is most likely to accept oxygen

118
Q

what does transferring electrons from a negative to a positive redox potential do

A

releases energy

119
Q

how is ATP formed from redox potentials

A

transferring electrons from a negative to a positive redox potential releases energy

Oxidative phosphorylation converts the energy inherent in these electrons into chemical energy in the form of ATP

GI (64 decks)

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