BMS1030 - Protein Metabolism Flashcards by Anya Anderson

What is catabolism, anabolism and metabolism?

Catabolism - breaking down
Anabolism - building up
Metabolism - mixture of both

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What is protein metabolism a source of?

Nitrogen and Energy

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What are the 3 stages of Protein metabolism called?

Transamination
Deamination
Transdeamination

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What feeds into the body’s amino acid pool (100g)

Dietary intake (50-80g)
Formation of non-essential AAs
Tissue breakdown

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How are amino acids in the body lost?

In urine (30g/day)
Tissue formation
Formation of non-protein nitrogenous substances (e.g. Purine, Pyrimidine, Creatine etc)
Synthesis of ATP (10% of calorie requirement)
Synthesis of carbohydrates

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Is protein stored in the body?

No - it is turned over all the time, always being broken down and made. If it isn’t used its broken down.

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What proteases are there in the GI tract and where?

Stomach - Pepsin

Pancreas
- Trypsin, Chymotrypsin, Elastase, Carboxypeptidase

Small Intestine - Aminopeptidase

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How are amino acids divided up?

Carbon skeleton and Amino group

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What metabolic intermediates is the AA carbon skeleton converted into?

Acetyl-CoA
Acetoacetyl-CoA
Pyruvate
Krebs cycle intermediates

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Where are most AAs metabolised? What is ammonia converted into?

In the liver
Ammonia -> Urea (for excretion)

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What are the key AAs in NH4+ (ammonia) metabolism?

Glutamine
Glutamate
Alanine
Aspartate

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Carbon skeletons enter the citric acid cycle via which intermediates?

In Krebs cycle:
a-ketoglutarate
Succinyl-CoA
Fumarate
Oxaloacetate (via Pyruvate)

To make ketone bodies:
Acetoacetyl-CoA
Acetyl-CoA (via Pyruvate and Acetoacetyl-CoA) - can also feed into Krebs cycle.

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Which 6 AAs go into forming pyruvate?

Alanine, Cysteine, Glycine, Serine, Threonine, Tryptophan

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Which 4 AAs go into forming Acetyl-CoA?

Isoleucine, Leucine, Threonine, Tryptophan

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Which 5 AAs go into forming Acetoacetyl-CoA?

Leucine, Lysine, Phenylalanine, Tryptophan, Tyrosine

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Tryptophan is very _____ to break down. Some parts of the molecule are used in synthesis of important compounds such as _________ - Vit B3.

complex
Nicotine

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What 4 AAs go into forming Glutamate and thus a-ketoglutarate?

Arginine, Glutamine, Histidine, Proline

What 4 AAs go into forming Succinyl-CoA?

Isoleucine, Methionine, Threonine, Valine

What 2 AAs go into forming fumarate?

Phenylalanine, Tyrosine

Pyruvate and which 2 AAs go into Oxaloacetate?

Asparagine, Aspartate

Asparagine –> Aspartate is a ________ reaction, catalysed by _________.

Deamination

Asparaginase

Aspartate –> oxaloacetate is achieved through ___________ with an a-ketoglutarate being aminated to a __________ at the same time.

Transamination

glutamate

In mammals, oxaloacetate is converted to ______ then transported into the ___________, where it can enter the TCA cycle.

malate
mitochondria

What is the difference between Glucogenic and Ketogenic?

Glucogenic: AA’s that can be converted into glucose (most AAs).

Ketogenic: AA’s that can only be converted into acetyl-CoA/acetoacetyl-CoA (exclusively lysine & leucine).

The body only synthesises limited amounts of ______________ amino acids, so it is better to have them in the _____ too.

non-essential diet

Describe Transamination

[An amino group is moved from one place to another.] 1. Aminotransferase remove the amino group on an AA to form a-keto acid, using coenzyme PLP. 2. a-ketoglutarate receives this amino group to form Glutamate.

Where is PLP derived from? What is its function?

Derived from vitamin B6. Function: to carry amino groups at active site of aminotransferases. (PLP is covalently bound to the enzyme at the active site).

What two forms does PLP exist as?

An aldehyde (CHO group) called pyridoxal phosphate. An amine (NH3+ group) called pyridoxamine phosphate. Aldehyde form is aminated when it accepts an NH3 group from the AA substrate.

In which cells is glutamate transported from the cytosol to mitochondria?

In hepatocytes (liver cells)

What occurs in deamination?

Enzyme Glutamate Dehydrogenase removes amino group from Glutamate molecule using H2O and NAD+/NADP+. a-ketoglutarate is re-formed. NH4+ enters the urea cycle. a-ketoglutarate enters Krebs cycle or used for glucose synthesis.

What is the effect of aminotransferase and glutamate dehydrogenase combined called?

Transdeamination

How is ammonia transported in the blood?

By first being converted to Glutamine.

How is ammonia converted into Glutamine?

- Glutamate aminated by Glutamine synthetase in liver. - Ammonia removed from hepatocyte mitochondria by glutaminase. - Glutamine is deaminated back to glutamate in liver mitochondria.

Summary of AA to Urea reactions

The Urea cycle and citric acid cycle are independent but they communicate via which intermediates?

Malate and Glutamate --> mitochondrial matrix Aspartate -> cytosol

What are the different coenzymes involved in transferring a C from AA substrates? What do they transfer the carbons as?

BIOTIN - contains O2 so highly oxidised - transfers carbon as CO2. S-ADENOSYLMETHIONINE - contains Hs so highly reduced - transfers carbon as -CH3 TETRAHYDROFOLATE - transfers carbon in several oxidation states. (note - the oxidised form is folate - vitamin B9) PLP can act as a cofactor in some 1-C transfer reactions.

Name 4 diseases that are results of errors in AA metabolism.

PKU Alkaptonuria MSUD MMA

What is PKU? - cause - symptoms - treatment

Phenylketonuria Defect in breakdown of Phenylalanine due to non-functioning phenylalanine hydroxylase. Phenylalanine and phenylpyruvate accumulate in blood and tissues -> impairing normal brain development. Phenyl-lactate gives urine 'mousy' odour. Babies now routinely screened for PKU. Patients prescribed diet low in phenylalanine.

Which sweetener is a source of phenylalanine?

Aspartame

What is Alkaptonuria? - cause -symptom

Build-up of homogentisate - an intermediate compound in the metabolism of tyrosine and phenylalanine. Turns urine black.

What is MSUD? - cause - symptoms - treatment

Defective branched-chain α-keto acid dehydrogenase (BCKD) enzyme complex. MSUD patients produce urine with a characteristic odour, due to build up of α-keto acids. Can result in abnormal brain development and death in early infancy. Rare disease. Treatment involves careful control of diet: limit intake of Val, Iso and Leu - which are not degraded in the liver.

What is MMA? - cause - symptom

Patients lack functioning methylmalonyl-CoA mutase enzyme. This leads to build up of toxic intermediate - similar to antifreeze poisoning. Rare genetic disease Treatment: protein-restricted diet