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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
Is the affinity of GLUT2 high or low for glucose?
Low affinity (only takes in glucose when in high concentrations)
26
How does glucose stimulate insulin secretion?
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
27
What polypeptide is insulin derived from?
Proinsulin
28
What is produced from the processing of proinsulin?
Insulin C peptide
29
How many disulfide bridges are in insulin?
3 - two between alpha and beta chains and one on the alpha chain
30
How many polypeptide chains is insulin made up of?
2
31
What can we use C peptide for?
Diagnostic purposes to see how much endogenous insulin is produced
32
What is the ratio of synthesis of C peptide to insulin?
1:1
33
What stimulates glucagon secretion?
Low blood glucose High blood amino acid concentration Adrenaline
34
Why is it important that high blood amino acid concentration stimulates glucagon secretion?
Prevents hypoglycaemia after a protein meal as brain and red blood cells need glucose
35
What are the metabolic effects of insulin? (3)
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
36
Describe the structure of an insulin receptor
Dimer Two alpha and two beta subunits Extracellular insulin binding site Intracellular tyrosine kinase
37
What are the three functions of the tyrosine kinase of the insulin receptor?
IRS docking site (insulin receptor substrate) Kinase activation Growth promoting activity
38
What does IRS stand for?
Insulin receptor substrate
39
What happens when insulin binds to its receptor? (IRS pathway)
Autophosphorylation of tyrosine residues on b-subunit IRS phosphorylated P13 kinase activated Phospholipids phosphorylated and kinase cascade leading to protein kinase B activated (phosphorylated)
40
On which subunit is the insulin binding site found?
Alpha
41
On which subunit is the tyrosine kinase found?
Beta
42
Describe how insulin affects glucose transport/storage in a muscle/fat cell (PKB)
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
43
Describe how insulin affects lipolysis in adipocytes (PKB)
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
Describe how insulin affects gene expression
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
Which glucose transporter is insulin-dependent?
GLUT4
46
What are the metabolic effects of glucagon?
(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
What are the metabolic effects of adrenaline?
Mobilises fuel during stress Stimulates glycogenolysis in muscle and liver Stimulates fatty acid release from adipose tissue
48
What are the metabolic effects of cortisol? (3)
(Provides for long-term requirements) Stimulates amino acid mobilisation from muscle Stimulates fatty acid release from adipose tissue Stimulates gluconeogenesis
49
What is the fed state?
When your body is digesting food and absorbing nutrients Lasts 2-4 hours after a meal
50
How do concentrations of nutrients in the blood change during the fed state?
Increase in blood glucose, amino acids and TAG (as chylomicrons)
51
Where does the liver get nutrients from?
Hepatic portal vein/supply
52
When is the liver engaged in gluconeogenesis?
At all times except during the fed state
53
What glucose transporter is found on liver cells?
GLUT2
54
What is the difference between glucokinase and hexokinase?
Glucokinase (liver) has a higher Km for glucose So does not compete with brain when blood glucose concentration is low
55
Which enzymes must be activated for glycolysis to occur (fed state)?
Glucokinase Phosphofructokinase Pyruvate kinase
56
How are the enzymes involved in glycogen synthesis/breakdown affected in the fed state?
Glycogen synthase activated Glycogen phosphorylase inhibited
57
How is fat metabolism in the liver affected in the fed state?
Fatty acid and TAG synthesis activated Acetyl CoA carboxylase activated (rate-limiting step)
58
What glucose transporter is present in the brain?
GLUT1
59
What glucose transporter is present on red blood cells?
GLUT1
60
Describe GLUT1
Present on brain and red blood cells Not insulin-dependent Low Km/high affinity Always takes up glucose
61
What occurs in muscle during the fed state?
Increased glucose uptake as increased GLUT4 Glycogenesis (same as liver) Amino acid uptake activated and increased protein synthesis
62
Where is glycogen synthesis activated during the fed state?
Liver Muscle
63
What occurs in adipose tissue in the fed state?
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
How much protein does the average man have?
6kg
65
How much protein can be lost before you die?
1/3
66
When do blood glucose levels peak?
1 hour after eating
67
When do blood glucose levels return to normal?
By 2 hours after eating
68
What happens to insulin and glucagon levels in the fasting state?
Insulin decreases Glucagon increases
69
What is the normal blood glucose concentration?
4mM
70
What is used in gluconeogenesis?
Lactate Glycerol Amino acids
71
What process generates all blood glucose 24 hours after eating?
Gluconeogenesis
72
Which tissue supplies the greatest source of energy in the fasting state?
Adipose tissue (TAG)
73
How are fatty acids transported in the bloodstream?
Bound to albumin
74
What substances activate hormone sensitive lipase in the fasting state?
Glucagon Adrenaline
75
What is the source of energy in muscles during the fasting state?
TAG No GLUT4 as no insulin
76
Why is it important that muscles do not use glucose during the fasting state?
So they do not compete with the brain
77
What happens to fatty acids in the liver during the fasting state?
Degraded to acetyl CoA (beta oxidation) Acetyl CoA converted to ketone bodies or used in TCA cycle
78
Why is muscle protein degraded during the fasting state?
Generate amino acids for gluconeogenesis in liver
79
What hormone activates the link reaction?
Insulin
80
What hormone inhibits the link reaction?
Glucagon
81
Why are fatty acids not gluconeogenic precursors?
Acetyl CoA cannot be converted back to pyruvate (to glucose)
82
Why does glucagon inhibit pyruvate dehydrogenase in the fasting state?
Inhibits the link reaction Ensures all gluconeogenic substrates are channelled into glucose production NOT acetyl CoA formation
83
Why does insulin activate pyruvate dehydrogenase in the fed state?
Activates link reaction Pyruvate --> acetyl CoA for fatty acid synthesis (acetyl CoA carboxylase also activated)
84
What are two examples of ketone bodies?
Acetoacetate b-hydroxybutyrate
85
Why can the brain use ketone bodies but not fatty acids?
Ketone bodies are smaller (and lipid-soluble) so can pass blood-brain barrier
86
Why is it important that the brain can use ketone bodies?
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
Why can urea excretion be used to measure gluconeogenesis?
Urea excretion is proportional to protein breakdown
88
What happens during starvation? (5)
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
How do people die from starvation? (3)
Fuel exhaustion Impairment of immune system - INFECTION Loss of function from loss of protein
90
What is a common infection that causes death during starvation and why?
Pneumonia Intercostal muscles damaged Cannot clear lungs
91
Approximately how long does it take to die from starvation?
40 days
92
How are each of the glucose tolerance curves of diabetics different to normal?
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
What percentage of the population in the UK is affected by diabetes mellitus?
2-3%
94
What is Type I diabetes often referred to as and why?
Insulin dependent diabetes mellitus/IDDM Insulin must be injected in order to survive
95
What is Type I diabetes?
Autoimmune destruction of b-cells
96
What are some of the symptoms of Type I diabetes?
HYPERLIPIDAEMIA KETOACIDOSIS Polyuria Polydipsia Polyphagia Fatigue Weight loss Muscle wasting Weakness
97
What is Type II diabetes often referred to as?
Non-insulin dependent diabetes mellitus/NIDDM
98
What is Type II diabetes?
Insulin resistance | Associated with diet and lifestyle
99
How does the metabolic pattern in uncontrolled diabetes relate to that of starvation?
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
What is found in the urine of diabetics (uncontrolled)?
Glucose Ketone bodies
101
What are the chronic complications of diabetes mellitus? (4)
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
How is Type I diabetes treated?
Exogenous insulin injections (must be balanced with food intake to prevent hypoglycaemia)
103
How is Type II diabetes treated?
Weight reduction Dietary modification Oral hypoglycaemic agents
104
What are the two hypoglycaemic agents used to treat Type II diabetes?
Biguanides Sulphonylureas
105
What do biguanides do?
Increase number of GLUT4
106
What do sulphonylureas do?
Act on b-cells to improve insulin secretion

BMS07 (7 decks)

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