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M104 T2 > M104 T2 L9 > Flashcards

M104 T2 L9 Flashcards

1
Q

What states does the human metabolism oscillate between?

A

the fed and fasting states

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2
Q

What is the ‘switch’ that determines metabolic changes?

A

the molar ratio of insulin to glucagon in the blood

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3
Q

When is the FED metabolic state in place?

A

during meals and for several hours afterwards

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4
Q

What are the FED and fasting metabolic states characterized by?

A

FED - high insulin and low glucagon (a high insulin/glucagon ratio)
fasting - low insulin and high glucagon (a low insulin/glucagon ratio)

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5
Q

When does the fasting metabolic state kick in?

A

6-12 hr after a meal

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6
Q

What is the criteria of ‘prolonged fasting’ or starvation?

A

fasting that lasts in excess of 12 hrs

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7
Q

What is the effect of food intake (FED state)?

A

stimulates insulin release
insulin inhibits glucagon secretion
this affects metabolism in the liver, muscle and adipose tissue
However, glucose utilization in the brain remains unchanged

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8
Q

What is the effect of high Cs of nutrients on the the insulin:glucagon ratio?

A

causes it to increase

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9
Q

What happens when there is a high blood glucose?

A

it enters the liver and is converted to glycogen and TGs
these are secreted as VLDL
some enters TCA cycle

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10
Q

What is glycerol from peripheral tissues converted into?

A

triacylglycerols

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11
Q

What happens to excess amacs entering from the gut?

A

they are converted to pyruvate and metabolised via the TCA cycle for energy or converted to triacylglycerols

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12
Q

How does glucose enter muscle tissue?

A

via the insulin-stimulated Glut 4 transport system

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13
Q

What happens to glucose once it has entered the muscle tissue?

A

it is converted to glycogen or metabolised via glycolysis and TCA cycle

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14
Q

How do FAs enter muscle tissue?

A 
via chylomicrons (if from the diet)
via VLDL (if from the liver) via VLDL. These
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15
Q

What are the two sources of FAs?

A

the diet

the liver

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16
Q

What happens to FAs once they enter muscle tissue?

A

they are oxidised via β-oxidation to acetyl CoA to produce ATP to support contraction

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17
Q

How does glucose enter adipose tissue?

A

via the insulin-dependent Glut 4 transport system

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18
Q

What happens to glucose once it enters adipose tissue?

A

it is converted into acetyl CoA and PDH via glycolysis

glucose < acetyl CoA and PDH < FAs < triacylglycerol

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19
Q

How do FAs enter adipose tissue?

A

via VLDL and chylomicrons

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20
Q

What happens to FAs once they enter adipose tissue?

A

it is converted to triacylglycerol

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21
Q

What happens to glycerol released from TGs?

A

it is returned to liver for re-use

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22
Q

What is the effect of insulin activity on LPL and HSL

activity?

A

LDL - is increased

HSL - is reduced

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23
Q

How does the brain take up glucose?

A

via Glut 1 & 3 transporters

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24
Q

What happens once glucose enters the brain?

A

it metabolises it oxidatively by glycolysis and the TCA cycle to produce ATP

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25
Q

How does the role of the liver change during fasting?

A

switches from a glucose-utilizing to a glucose-producing organ
there is a decrease in glycogen synthesis and an increase in glycogenolysis

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26
Q

What happens as plasma glucose falls?

A

glucose no longer enters liver as Glut 2 transporter has low affinity

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27
Q

What is the effect of a reduced insulin: glucagon ratio?

A

it activates glycogenolysis and gluconeogenesis (from lactate and alanine) via cAMP production in response to glucagon

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28
Q

What are FAs from lipolysis used for?

A

to produce E via b-oxidation

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29
Q

What is citrate and acetyl CoA produced from?

A

from the oxidation of FAs - this activates gluconeogenesis and inhibits glycolysis

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30
Q

What is the effect in reduced insulin levels?

A

it reduces glucose entry into muscle tissue

glycogenolysis does not occur as there are no glucagon receptors in skeletal muscle to cause activation

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31
Q

When insulin levels are low, what is used as an alternative E source?

A

muscle and other peripheral tissues switch to FA oxidation as a source of E
this inhibits glycolysis and glucose utilisation

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32
Q

In the early fasting state, what happens to proteins

A

they are broken down to amacs
the carbon skeletons can be used for E
or exported to the liver in the form of alanine

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33
Q

What is the entry of glucose into adipose tissue via the Glut 4 transport system reduced in response to?

A

in response to the lowered insulin and metabolism of glucose via glycolysis being severely inhibited

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34
Q

What does the mobilisation of TGs occur in response to?

A

in response to the reduced insulin:glucagon ratio and activation of the sympathetic NS by release of noradrenaline

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35
Q

What are FAs used for in adipose tissue?

A

used directly within the tissue to produce energy

the remainder are released into the bloodstream to support glucose-independent E production in muscle and other tissues

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36
Q

What happens to glycerol in adipose tissue?

A

it cannot be metabolised so it is recycled to the liver to support gluconeogenesis

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37
Q

How does the brain continue to take up glucose in the early fasting state?

A

bc of the high affinity of Glut1 and Glut3 transport system and independence from insulin
so glucose continues to be metabolised despite the fact that no glucose is provided in the diet

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38
Q

Why does the brain continue to take up glucose in the early fasting state rather than using alternatives?

A

bc the brain can’t switch to FAs as a source of fuel as free FAs don’t cross the blood brain barrier

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39
Q

What is the metabolism like in the starved state?

A

Chronic low-insulin, high glucagon state

40
Q

What happens to hormone levels in the starved state?

A

the concentration of thyroid hormones decreases, which decreases the metabolic rate

41
Q

What is the major E source in the starved state?

A

Free FAs

the production of ketone bodies is an alternative fuel source

42
Q

How is absorption of the liver affected in the starved state?

A

no glucose enters liver and glycogen stores are depleted within 24 hours

43
Q

In the starved state, what is the plasma glucose dependent on?

A

gluconeogenesis from lactate, glycerol & alanine from fat and protein breakdown
the kidney also becomes an important source of gluconeogenesis

44
Q

In the starved state, why is the synthesis of urea stimulated?

A

to cope with increasing amacs entering liver

45
Q

What processes are inhibited under the starved state?

A

Glycogen synthesis and glycolysis

46
Q

What is the role of FAs in the liver under the starved state?

A

they provide E to support gluconeogenesis with excess acetyl CoA being converted to ketone bodies

47
Q

What ketone bodies is excess acetyl CoA converted into in gluconeogenesis of the liver?

A

acetoacetate and β-hydroxybutyrate

48
Q

What are ketone bodies in the starved state, located in the liver, used for?

A

they are released for oxidation by other tissues

49
Q

What happens to muscle glucose in the starved state?

A

glucose entry is reduced with a fall in insulin

FAs are used instead as the fuel

50
Q

What happens to ketone bodies in the starved state?

A

they are taken up by muscle and other peripheral tissues

they are used as a further source of fuel in heart and muscle conserving glucose

51
Q

What are the effects of the actions of ketone bodies in the starved state?

A

they reduce proteolysis and decrease muscle wasting

52
Q

What does muscle tissue use for the E to contract in the starved state?

A

FA oxidation

53
Q

What is the first stage of the glucose-fatty acid cycle?

A

glucagon or adrenaline causes the mobilisation of FAs this increases FA oxidation to acetyl CoA in peripheral tissues

54
Q

What is the second stage of the glucose-fatty acid cycle, involves acetyl CoA?

A

Excess acetyl CoA converted to citrate in TCA cycle which builds up in cytoplasm and inhibits PFK-1

55
Q

What is the third stage of the glucose-fatty acid cycle, involves acetyl CoA?

A

Build up of G-6-P inhibits hexokinase and prevents glucose phosphorylation

56
Q

What is the fourth stage of the glucose-fatty acid cycle, involves acetyl CoA?

A

Increase in glucose prevents further glucose entry and so conserves glucose

57
Q

What happens to adipose glucose in the starved state?

A

glucose entry is reduced with a fall in insulin

FAs from triacylglycerol are used as fuel for all the major tissues

58
Q

What process is greatly activated in adipose tissue in the starved state and what causes it?

A

Lipolysis

bc the low insulin:glucagon ratio and blood levels of FAs rise 10-fold

59
Q

What happens to adipose glycerol in the starved state?

A

it is exported to the liver to be converted into glucose

60
Q

What happens to the brain in the starved state?

A

limited levels of glucose for the brain to use
as the levels of ketone bodies rise in the plasma, FAs can cross the blood brain barrier and enter the brain as a source of E, even though FAs can’t be used by the brain

61
Q

How are ketone bodies used by the brain in the starved state?

A

they can’t completely make up for glucose, so the brain still needs to take it up glucose and metabolise via glycolysis
maintaining net glucose synthesis during starvation is essential

62
Q

What happens to ketone body concentration during fasting or starvation?

A

it increases

63
Q

What concentration of plasma ketone bodies is sufficient to allow use by the CNS? When does this occur?

A

4mM+

occurs after approx. 3 days of starvation

64
Q

What is glucose sourced by across the different metabolic states?

A

Fed state - diet
Fasted state - most from the breakdown of liver glycogen, increasing amounts by gluconeogenesis
Starved state - most from gluconeogenesis

65
Q

What are enzymes involved in glycogenolysis / glycogen synthesis regulated by?

A

allosteric control

hormonal control

66
Q

What are examples of hormones responsible for regulating enzymes involved in glycogenolysis / glycogen synthesis?

A

glucagon, adrenaline, cortisol and insulin

67
Q

What is hormonal control of enzymes regulated by?

A

phosphorylation

68
Q

Where is glucagon released from?

A

pancreatic α-cells

69
Q

What is the initiator of glucagon release?

A

hypoglycaemia

70
Q

What is the effect of glucagon and adrenaline on glycogenolysis/ gluconeogenesis?

A

rapid activation

71
Q

Where is adrenaline and coritsol released from?

A

adrenal medulla

72
Q

What is the initiator of adrenaline release?

A

stress and hypoglycaemia

73
Q

What is the initiator of coritsol release?

A

stress

74
Q

What is the effect of coritsol on glycogenolysis/ gluconeogenesis?

A

chronic activation

75
Q

What is the initiator of insulin release?

A

hyperglycaemia

76
Q

Where is insulin released from?

A

pancreatic β-cells

77
Q

What is the effect of insulin on glycogenolysis/ gluconeogenesis?

A

inactivation

78
Q

What triggers insulin release?

A

increased bgc, promoting glucose oxidation, glycogen synthesis and TG synthesis

79
Q

What triggers glucagon and adrenaline release?

A

low bgc

releases glucose from glycogen in the liver to increase it

80
Q

What is another name for adrenaline?

A

epinephrine

81
Q

What happens to adrenaline levels during exercise?

A

its levels rise greatly during exercise when glycogen breakdown is required to support muscle contraction

82
Q

How does glucagon (liver) and adrenaline (muscle) activate glycogen breakdown and inhibit synthesis?

A

by activating cAMP PK with ultimate phosphorylation of phosphorylase and glycogen synthase
Mimicked by increasing Ca2+ during contraction
Insulin activates protein phosphatase to reverse these effects

83
Q

What are the effects of glucagon (liver) and adrenaline (muscle)?

A

they activate glycogen breakdown and inhibit synthesis

they increase cAMP production and activate cAMP PK

84
Q

What is the effect of the activation of cAMP PK?

A

it phosphorylates glycogen synthase switching it OFF
it phosphorylates phosphorylase kinase leading to activation

Phosphorylase kinase can also phosphorylate glycogen synthase ensuring it is inactive

85
Q

What two substances does cAMP PK phosphorylate?

A

glycogen synthase

phosphorylase kinase

86
Q

What is the effect of phosphorylating glyocgen synthase?

A

it is switched off - inactivated

87
Q

What is the effect of phosphorylating phosphorylase kinase?

A

it is switched on - activated

88
Q

What are the two forms of phosphorylase kinase?

A

active “a” form - is phosphorylated

inactive “b” form - is not phosphorylated

89
Q

What is the role of phosphorylase kinase?

A

it phosphorylates Phosphorylase, switching it ON

90
Q

What happens when Phosphorylase is activated?

A

glycogen degradation occurs

glycogen synthesis is inhibited

91
Q

What substances activate Phosphorylase kinase?

A

glucagon

Ca2+ ions (allosterically)

92
Q

How is Phosphorylase kinase activated by Ca2+ ions?

A

links muscle contraction with glycogen breakdown ensuring adequate ATP

93
Q

What is the effect of insulin on protein phosphatase -1?

A

it activates it, which removes the phosphates from phosphorylase, glycogen synthase and phosphorylase kinase
this switches OFF glycogen breakdown and switches ON glycogen synthesis

94
Q

How does glucagon stimulate glycogenolysis?

A

via the 2nd messenger cAMP in the liver

95
Q

How does adrenaline stimulate glycogenolysis?

A

the 2nd messenger cAMP and Ca2+ in the liver and muscles

via b-adrenergic receptors and a1-adrenergic

96
Q

What is the role of LPL in adipose tissue?

A

it controls lipid uptake into the adipose tissue

its activity is increased by insulin

97
Q

Does glucagon affect muscle tissue and why?

A

no becuase muscle cells don’t have glucagon receptors

M104 T2 (15 decks)

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