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Yr 2 - GI & Metabolism > Protein Metabolism > Flashcards

Protein Metabolism Flashcards

1
Q

What is the use of amino acids in the body?

A
  1. Protein synthesis
  2. Synthesis of nitrogen containing metabolites
  3. Energy (ATP)
  4. Fatty acids, ketone bodies
  5. Glucose/glycogen
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2
Q

What nitrogen containing compounds can these amino acids be turned into:

  1. Glycine
  2. Tyrosine
  3. Tryptophan
  4. Histidine
  5. Glycine/arginine
  6. Glycine, aspartate, glutamine
A
  1. Haem
  2. Dopamine, noradrenalin, adrenalin (catecholamines)
  3. Serotonin
  4. Histamine
  5. Creatine
  6. Purine bases
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3
Q

What are the signs and symptoms of malnutrition?

A
  • Poor growth
  • Susceptibility to infection
  • Changes in hair/skin colour
  • Poor skin condition and poor nutrient absorption
  • Abdominal bloating
  • Lower limb oedema
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4
Q

How does a lack of protein lead to susceptibility to infection?

A

Antibodies are proteins

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5
Q

How does a lack of protein lead to poor growth?

A

Need protein for DNA, ATP etc

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6
Q

How does a lack of protein lead to changes in hair/skin colour?

A

Insufficient melanin

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7
Q

How does a lack of protein lead to poor skin condition and poor nutrient absorption?

A

Epithelial cells have high turnover rate –> inability to replace leads to poor condition of skin

Epithelial cells also line gut, leading to problems with absorption

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8
Q

How does a lack of protein lead to lower limb oedema?

A

Lack of albumin (blood protein) –> fluid is retained and oedema occurs

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9
Q

How does a lack of protein lead to abdominal bloating?

A

Reduced albumin due to protein deficiency –> fluid accumulates in tissues, causing build up in abdomen

Accumulation of fat in liver

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10
Q

If amino acids are not required for synthetic reactions, what can they be used for? What must occur for this to happen?

A

Used for energy, or converted to energy storage compounds

Amino group must be removed and nitrogen excreted

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11
Q

Why must blood ammonia levels be kept low?

A

Ammonia is very toxic

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12
Q

What can hyperammonaemia lead to?

A

Tremor, vomiting, cerebral oedema, coma, death

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13
Q

What can hyperammonaemia be caused by?

A

Genetic defects (e.g. deficiencies of urea cycle enzymes)

More commonly caused by liver disease (hepatitis or cirrhosis)

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14
Q

How is ammonia excreted?

A

Converted to urea for excretion by the kidneys

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15
Q

What are the 3 steps in the excretion of urea?

A
  1. Transamination
  2. Deamination
  3. Urea synthesis
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16
Q

What is step 1 - transamination?

A

Transfer of amino group from amino acid to a-ketoglutarate to form glutamate (in most tissues)

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17
Q

What is step 2 - deamination?

A

Release of ammonia from glutamate (reverse)

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18
Q

Where does step 2 - deamination - mainly happen?

A

Liver

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19
Q

What is step 3 - urea synthesis?

A

Urea cycle (in liver)

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20
Q

How can ammonia be safely transported to the liver?

A

As glutamate or glutamine

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21
Q

What does step 1 (transamination) require?

A

Pyridoxal phosphate

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22
Q

What is pyridoxal phosphate?

A

The active form of vitamin B6

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23
Q

What can a lack of vitamin B6 lead to?

A
  • Anaemia (lack of haem)
  • Neurological symptoms (lack of neurotransmitter and lipid synthesis)
  • Poor growth, skin lesions, poor immune responses (lack of protein synthesis)
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24
Q

What is vitamin B6 required for?

A
  1. Transamination and synthesis of non-essential amino acids
  2. Decarboxylation reactions required for neurotransmitter synthesis
  3. Haem synthesis
  4. Some aspects of energy metabolism & lipid synthesis
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25
What is the control step in urea synthesis?
Carbamoyl phosphate synthesis
26
What synthesises carbamoyl phosphate? What is this enzymes activated by?
Carbamoyl phosphate synthetase 1 Is allosterically activated by N-acetylglutamate
27
When is N-acetylglutamate formed?
When glutamate levels are high
28
What does high glutamate levels signal?
High levels of protein catabolism
29
What is the speed of the urea cycle determined by?
The amount of amino acids (activated by high levels of amino acids)
30
Where does the urea cycle take place?
Partly in the mitochondrial matrix and partly in the cytosol
31
Describe the urea cycle inside the mitochondrial matrix
- Carbamoyl phosphate formed from ammonia and bicarbonate – control step - Carbamoyl group transferred to ornithine to form citrulline
32
Describe the urea cycle in the cytosol
- Second amino group added from aspartate - Arganine formed and hydrolysed - Urea released
33
What does uric acid contain?
Nitrogen
34
What is uric acid derived from?
Purine nucleotides rather than proteins
35
What is excess uric acid in the blood called?
Hyperuricaemia
36
What can hyperuricaemia lead to?
Deposition of sodium urate crystals in the kidneys and in the joints
37
What are deposits of sodium urate crystals in the kidneys called?
Kidney stones
38
What are deposits of sodium urate crystals in the joints called?
Gout
39
What is hyperuricaemia caused by?
Over-production of urate, or poor excretion via the kidneys
40
What are high purine foods?
Red meat, seafood, yeast-containing foods
41
What can the carbon skeleton of amino acids be fed into?
Several metabolic pathways: - Krebs cycle (used to synthesis ATP) - Fatty acid and ketone synthesis - Glucose synthesis (gluconeogenesis)
42
What amino acids cannot be made into glucose? Why?
Lycine and Leucine Only enter the cycle via acetyl CoA
43
Describe Lycine and Leucine
Solely ketogenic --> can only be made into Acetyl CoA and ketone bodies
44
What are glucogenic amino acids?
Can be degraded to glucose precursors
45
What are ketogenic amino acids?
Can be degraded to precursors of fatty acids and ketone bodies
46
Can acetyl CoA be converted to glucose?
No
47
What is gluconeogenesis?
Making glucose from non-carbohydrate intermediates (during fasting or exercise)
48
Where does gluconeogenesis mainly take place?
In the cytosol of the liver and kidney
49
Gluconeogenesis takes place from what precursors?
- Keto acids (derived from amino acids particularly alanine) - Lactate (from anaerobic glycolysis) - Glycerol (from triacylglycerol breakdown)
50
What is gluconeogenesis vital for?
Maintaining blood glucose levels as glycogen stores only last about 18 hours
51
Gluconeogenesis is mainly a reversal of glycolysis (but there are 3 irreversible steps in glycolysis, therefore different enzymes are required for reversal). What 3 steps in gluconeogenesis are catalysed by different enzymes to glycolysis?
1. Pyruvate --> phosphoenolpyruvate (requires several stages) 2. Fructose 1,6 bisphosphate --> fructose 6 phosphate (fructose 1,6 bisphosphatase) 3. Glucose 6 phosphate --> glucose (glucose 6 phosphatase)
52
How is gluconeogenesis and glycolysis controlled?
- High glucose and/or low energy = glycolysis | - Low glucose and/or high energy = gluconeogenesis
53
What is glycolysis activated by?
AMP, ADP (suggests low energy) Insulin
54
What is glycolysis inhibited by?
ATP | Glucagon
55
What is gluconeogenesis activated by?
Citrate Glucagon Acetyl CoA
56
What is glyconeogenesis inhibited by?
AMP, ADP (suggests low energy) | Insulin
57
What is not produced in type 1 diabetes?
Insulin
58
What is effect of type 1 diabetes on glycolysis?
Glycolysis is inhibited (insulin is also required to allow glucose entry to muscle and adipose tissue) Blood glucose levels rise
59
Where is insulin released from?
Pancreas
60
What is effect of type 1 diabetes on gluconeogenesis?
Is stimulated --> the liver synthesises and releases glucose into the circulation Blood glucose levels rise further
61
In type 1 diabetes, in order to provide substrates for gluconeogenesis, what happens?
Muscle protein is broken down to provide amino acids --> rapid weight loss
62
Describe function of liver during exercise
- Anaerobic respiration - Lactate production - Lactate removed (so glycolysis can continue) - Lactate travels to liver - Lactate converted back into glucose by gluconeogenesis which can then be released again for muscles
63
Why does alcohol make you hungry?
- Ethanol is metabolised in the liver - Produces large amounts of NADH so lowers levels of NAD+ - NADH inhibits gluconeogenesis and lowers blood glucose (hungry) Pyruvate and alanine is converted to lactate instead of glucose in presence of lots of NADH Alanine --> pyruvate --> lactate

Yr 2 - GI & Metabolism (51 decks)

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