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BMS07 > Integration of Metabolism > Flashcards

Integration of Metabolism Flashcards

1
Q

How can changes in metabolic pattern be achieved? (4)

A

Variation in amount of available substrate

Allosteric enzyme regulation

Covalent modification of enzymes

Changes in enzyme synthesis

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2
Q

What are the main hormones controlling intermediary metabolism?

A

Insulin

Glucagon

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3
Q

What type of hormone is insulin? (relating to glucose)

A

The only hypoglycaemic hormone

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4
Q

What type of hormone is glucagon? (relating to glucose)

A

Hyperglycaemic

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5
Q

What are some other insulin counter-regulatory hormones other than glucagon?

A

Adrenaline

Cortisol

Growth hormone

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6
Q

Where is adrenaline produced?

A

Adrenal medulla

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7
Q

Where is cortisol produced?

A

Adrenal cortex

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8
Q

Where is growth hormone produced?

A

Anterior pituitary

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9
Q

What do the islets of Langerhans make up?

A

Endocrine part of pancreas

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10
Q

What do b-cells secrete?

A

Insulin

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11
Q

What do a-cells secrete?

A

Glucagon

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12
Q

What cells secrete insulin?

A

b-cells

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13
Q

What cells secrete glucagon?

A

a-cells

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14
Q

How much of the total pancreatic mass is made up of islets of Langerhans?

A

2%

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15
Q

How many islets are in the average human pancreas?

A

1 million

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16
Q

Where are islets of Langerhans found?

A

Pancreas

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17
Q

What percentage of islets are b-cells?

A

60-70%

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18
Q

What percentage of islets are a-cells?

A

30-40%

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19
Q

What do δ-cells secrete?

A

Somatostatin

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20
Q

What stimulates insulin secretion? (4)

A

Rise in blood glucose

Rise in blood amino acids (weaker influence)

Gut hormones

Glucagon

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21
Q

What gut hormones stimulate insulin secretion?

A

Secretin and other GI hormones released after food intake, before blood glucose is elevated

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22
Q

Why is it beneficial that glucagon stimulates insulin release?

A

Allows fine tuning of glucose homeostasis (prevent large fluctuations)

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23
Q

What inhibits insulin secretion?

A

Adrenaline

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24
Q

What glucose transporter is found on b-cells?

A

GLUT2

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25
Q

Is the affinity of GLUT2 high or low for glucose?

A

Low affinity (only takes in glucose when in high concentrations)

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26
Q

How does glucose stimulate insulin secretion?

A

Glucose enters cell via GLUT2

Metabolised to ATP

K+ channel closed so no K+ in

Voltage-gated Ca2+ channel opens and intracellular Ca2+ concentration increases

Insulin released from vesicles

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27
Q

What polypeptide is insulin derived from?

A

Proinsulin

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28
Q

What is produced from the processing of proinsulin?

A

Insulin

C peptide

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29
Q

How many disulfide bridges are in insulin?

A

3 - two between alpha and beta chains and one on the alpha chain

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30
Q

How many polypeptide chains is insulin made up of?

A

2

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31
Q

What can we use C peptide for?

A

Diagnostic purposes to see how much endogenous insulin is produced

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32
Q

What is the ratio of synthesis of C peptide to insulin?

A

1:1

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33
Q

What stimulates glucagon secretion?

A

Low blood glucose

High blood amino acid concentration

Adrenaline

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34
Q

Why is it important that high blood amino acid concentration stimulates glucagon secretion?

A

Prevents hypoglycaemia after a protein meal as brain and red blood cells need glucose

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35
Q

What are the metabolic effects of insulin? (3)

A

Promotes fuel storage after a meal

  • Stimulates glycogenesis
  • Stimulates fatty acid synthesis and storage from carbohydrates when glycogen capacity exceeded

Promotes growth

Stimulates amino acid uptake and protein synthesis

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36
Q

Describe the structure of an insulin receptor

A

Dimer

Two alpha and two beta subunits

Extracellular insulin binding site

Intracellular tyrosine kinase

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37
Q

What are the three functions of the tyrosine kinase of the insulin receptor?

A

IRS docking site (insulin receptor substrate)

Kinase activation

Growth promoting activity

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38
Q

What does IRS stand for?

A

Insulin receptor substrate

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39
Q

What happens when insulin binds to its receptor? (IRS pathway)

A

Autophosphorylation of tyrosine residues on b-subunit

IRS phosphorylated

P13 kinase activated

Phospholipids phosphorylated and kinase cascade leading to protein kinase B activated (phosphorylated)

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40
Q

On which subunit is the insulin binding site found?

A

Alpha

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41
Q

On which subunit is the tyrosine kinase found?

A

Beta

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42
Q

Describe how insulin affects glucose transport/storage in a muscle/fat cell (PKB)

A

Protein kinase B promotes GLUT4 (translocation) so more glucose taken in

Protein kinase B phosphorylates glycogen synthase kinase = inactivated

Glycogen synthase remains active (not inhibited by GSK) so more glycogenesis

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43
Q

Describe how insulin affects lipolysis in adipocytes (PKB)

A

Protein kinase B phosphorylates phosphodiesterase = active

Phosphodiesterase converts cAMP to 5’AMP

No cAMP available to activate protein kinase A

Hormone sensitive lipase not activated so TAG not hydrolysed

44
Q

Describe how insulin affects gene expression

A

Insulin binding and autophosphorylation of tyrosine residues

Protein scaffold results in Ras-GTP being formed (activated)

Kinase phosphorylation cascade results in activation of MAP kinase

MAP kinase alters activity of transcription factors

45
Q

Which glucose transporter is insulin-dependent?

A

GLUT4

46
Q

What are the metabolic effects of glucagon?

A

(Mobilises fuel and maintains blood glucose during fasting)

Activates glycogenolysis and gluconeogenesis (and amino acid uptake) in liver

Activate fatty acid release from adipose tissue

Activate fatty acid oxidation and ketogenesis in liver

47
Q

What are the metabolic effects of adrenaline?

A

Mobilises fuel during stress

Stimulates glycogenolysis in muscle and liver

Stimulates fatty acid release from adipose tissue

48
Q

What are the metabolic effects of cortisol? (3)

A

(Provides for long-term requirements)

Stimulates amino acid mobilisation from muscle

Stimulates fatty acid release from adipose tissue

Stimulates gluconeogenesis

49
Q

What is the fed state?

A

When your body is digesting food and absorbing nutrients

Lasts 2-4 hours after a meal

50
Q

How do concentrations of nutrients in the blood change during the fed state?

A

Increase in blood glucose, amino acids and TAG (as chylomicrons)

51
Q

Where does the liver get nutrients from?

A

Hepatic portal vein/supply

52
Q

When is the liver engaged in gluconeogenesis?

A

At all times except during the fed state

53
Q

What glucose transporter is found on liver cells?

A

GLUT2

54
Q

What is the difference between glucokinase and hexokinase?

A

Glucokinase (liver) has a higher Km for glucose

So does not compete with brain when blood glucose concentration is low

55
Q

Which enzymes must be activated for glycolysis to occur (fed state)?

A

Glucokinase

Phosphofructokinase

Pyruvate kinase

56
Q

How are the enzymes involved in glycogen synthesis/breakdown affected in the fed state?

A

Glycogen synthase activated

Glycogen phosphorylase inhibited

57
Q

How is fat metabolism in the liver affected in the fed state?

A

Fatty acid and TAG synthesis activated

Acetyl CoA carboxylase activated (rate-limiting step)

58
Q

What glucose transporter is present in the brain?

A

GLUT1

59
Q

What glucose transporter is present on red blood cells?

A

GLUT1

60
Q

Describe GLUT1

A

Present on brain and red blood cells

Not insulin-dependent

Low Km/high affinity

Always takes up glucose

61
Q

What occurs in muscle during the fed state?

A

Increased glucose uptake as increased GLUT4

Glycogenesis (same as liver)

Amino acid uptake activated and increased protein synthesis

62
Q

Where is glycogen synthesis activated during the fed state?

A

Liver

Muscle

63
Q

What occurs in adipose tissue in the fed state?

A

Lipoprotein lipase activated by insulin allows fatty acids to enter adipocytes

Glucose uptake increased due to increased GLUT4 for glycerol phosphate production

TAG stored

Hormone sensitive lipase inhibited by insulin

64
Q

How much protein does the average man have?

A

6kg

65
Q

How much protein can be lost before you die?

A

1/3

66
Q

When do blood glucose levels peak?

A

1 hour after eating

67
Q

When do blood glucose levels return to normal?

A

By 2 hours after eating

68
Q

What happens to insulin and glucagon levels in the fasting state?

A

Insulin decreases

Glucagon increases

69
Q

What is the normal blood glucose concentration?

A

4mM

70
Q

What is used in gluconeogenesis?

A

Lactate

Glycerol

Amino acids

71
Q

What process generates all blood glucose 24 hours after eating?

A

Gluconeogenesis

72
Q

Which tissue supplies the greatest source of energy in the fasting state?

A

Adipose tissue (TAG)

73
Q

How are fatty acids transported in the bloodstream?

A

Bound to albumin

74
Q

What substances activate hormone sensitive lipase in the fasting state?

A

Glucagon

Adrenaline

75
Q

What is the source of energy in muscles during the fasting state?

A

TAG

No GLUT4 as no insulin

76
Q

Why is it important that muscles do not use glucose during the fasting state?

A

So they do not compete with the brain

77
Q

What happens to fatty acids in the liver during the fasting state?

A

Degraded to acetyl CoA (beta oxidation)

Acetyl CoA converted to ketone bodies or used in TCA cycle

78
Q

Why is muscle protein degraded during the fasting state?

A

Generate amino acids for gluconeogenesis in liver

79
Q

What hormone activates the link reaction?

A

Insulin

80
Q

What hormone inhibits the link reaction?

A

Glucagon

81
Q

Why are fatty acids not gluconeogenic precursors?

A

Acetyl CoA cannot be converted back to pyruvate (to glucose)

82
Q

Why does glucagon inhibit pyruvate dehydrogenase in the fasting state?

A

Inhibits the link reaction

Ensures all gluconeogenic substrates are channelled into glucose production NOT acetyl CoA formation

83
Q

Why does insulin activate pyruvate dehydrogenase in the fed state?

A

Activates link reaction

Pyruvate –> acetyl CoA for fatty acid synthesis (acetyl CoA carboxylase also activated)

84
Q

What are two examples of ketone bodies?

A

Acetoacetate

b-hydroxybutyrate

85
Q

Why can the brain use ketone bodies but not fatty acids?

A

Ketone bodies are smaller (and lipid-soluble) so can pass blood-brain barrier

86
Q

Why is it important that the brain can use ketone bodies?

A

Results in up to 40% reduction in glucose demand of brain

Less muscle protein degraded as less gluconeogenesis required

Loss of 1/3 of body protein = death

87
Q

Why can urea excretion be used to measure gluconeogenesis?

A

Urea excretion is proportional to protein breakdown

88
Q

What happens during starvation? (5)

A

More ketone bodies recovered from kidneys

Muscle uses fatty acids

Fatty acid concentrations plateau and ketone bodies rise

Brain uses more ketone bodies and less glucose

Urea production decreases

89
Q

How do people die from starvation? (3)

A

Fuel exhaustion

Impairment of immune system - INFECTION

Loss of function from loss of protein

90
Q

What is a common infection that causes death during starvation and why?

A

Pneumonia

Intercostal muscles damaged

Cannot clear lungs

91
Q

Approximately how long does it take to die from starvation?

A

40 days

92
Q

How are each of the glucose tolerance curves of diabetics different to normal?

A

Type I: starts much higher and does not decrease back to ‘normal’ level

Type II: starts higher and takes longer to reach ‘normal’ level

93
Q

What percentage of the population in the UK is affected by diabetes mellitus?

A

2-3%

94
Q

What is Type I diabetes often referred to as and why?

A

Insulin dependent diabetes mellitus/IDDM

Insulin must be injected in order to survive

95
Q

What is Type I diabetes?

A

Autoimmune destruction of b-cells

96
Q

What are some of the symptoms of Type I diabetes?

A

HYPERLIPIDAEMIA

KETOACIDOSIS

Polyuria

Polydipsia

Polyphagia

Fatigue

Weight loss

Muscle wasting

Weakness

97
Q

What is Type II diabetes often referred to as?

A

Non-insulin dependent diabetes mellitus/NIDDM

98
Q

What is Type II diabetes?

A

Insulin resistance

Associated with diet and lifestyle

99
Q

How does the metabolic pattern in uncontrolled diabetes relate to that of starvation?

A

Much more exaggerated

No insulin (starvation= low insulin) so glucagon acts unopposed

Muscle protein breakdown and fatty acids release continue and uncontrolled ketogenesis (starvation = ketone bodies stimulate release of insulin to limit these processes)

100
Q

What is found in the urine of diabetics (uncontrolled)?

A

Glucose

Ketone bodies

101
Q

What are the chronic complications of diabetes mellitus? (4)

A

Microangiopathy (thickening of basement membrane)

Retinopathy (blindness is 25x more common)

Nephropathy (renal failure is 17x more common)

Neuropathy (postural hypotension, impotence, foot ulcers)

102
Q

How is Type I diabetes treated?

A

Exogenous insulin injections (must be balanced with food intake to prevent hypoglycaemia)

103
Q

How is Type II diabetes treated?

A

Weight reduction

Dietary modification

Oral hypoglycaemic agents

104
Q

What are the two hypoglycaemic agents used to treat Type II diabetes?

A

Biguanides

Sulphonylureas

105
Q

What do biguanides do?

A

Increase number of GLUT4

106
Q

What do sulphonylureas do?

A

Act on b-cells to improve insulin secretion

BMS07 (7 decks)

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