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BVetMed3 - PMVPH > Biochemical Consequences Of Protein And Energy Imbalances > Flashcards

Biochemical Consequences Of Protein And Energy Imbalances Flashcards

1
Q

What are the three key foodstuffs that omnivores from the gut?

A

Glucose

Amino acids

Long chain fatty acids

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2
Q

What happens to most glucose once it is absorbed in omnivores?

A

80% taken is taken up into muscle cells and stored as glycogen

20% goes to liver - glycogen

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3
Q

How is glucose taken up into muscle cells?

A

Insulin dependent system of uptake

GLUT4 transporters on membrane

Insulin released when glucose is high therefore GLUT4 allows glucose into muscle cells when glucose is high

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4
Q

How is glucose taken into liver cells?

A

GLUT2 transporter

Has a very high Km therefore only works at very high concentrations of glucose.

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5
Q

Where are GLUT-2 transporters found?

A

Hepatocytes

B cells in pancreas

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6
Q

What happens to glucose which is not converted into glycogen?

A

Respiration

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7
Q

What happens when there is excess Acetyl CoA ?

A

Converted into long-chain fatty acids through fatty acid synthesis

Stored in adipocytes

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8
Q

How does insulin exert its effect?

A

Brings about a signalling cascade leading to the DEPHOSPHORYLATION of a series of regulatory enzymes.

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9
Q

How does glucagon exert its effect?

A

Leads to the phosphorylation of the same enzymes as insulation - like an off switch.

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10
Q

Other than glycogen, how can glucose be stored?

A

Go to adipocytes and is made into glycerol

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11
Q

How can fatty acids be sourced?

A

Excess Acetyl CoA

Absorbed from gut as chylomicrons - enter tissues where a lipase extracts the fats.

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12
Q

What happens to fatty acids once they enter adipocytes?

A

Fats are esterified with glycerol to make triglycerides for storage

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13
Q

What happens if there are high levels of fatty acids?

A

Converted into Acetyl CoA and enter the CAC

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14
Q

How can amino acids be utilised?

A

Versatile metabolic substrates

When you delaminates them you can use them for lots of different purposes including converting them into PYRUVATE, ACETYL COA, and OAA

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15
Q

Other than for metabolism, how can amino acids be utilised?

A

Put into muscle protein.

Can also be taken and used as a metabolic intermediate when low glucose.

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16
Q

How do the main nutrients absorbed by omnivores and carnivores differ?

A

The main nutrient absorbed by carnivores is AMINO ACIDS

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17
Q

What are the two types of amino acid?

A

Glucogenic
Can be converted to pyruvate or oxaloacetate

Ketogenic
Can be converted to Acetyl CoA

(NB SOME CAN DO BOTH)

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18
Q

How does glucagon exert its effect?

A

Low blood sugar
Release of glucagon from alpha cells

Binds to receptor on responsive tissue
- Adenyly cyclise - cAMP- PKA activated - phosphorylation of regulatory enzymes

19
Q

What are the key energy sources for fasting omnivores?

How are they sourced?

How do they provide an energy source?

A

Fatty acids

Triglycerides in adipocytes broken down to long chain fatty acids

Fatty acids converted to Acetyl CoA

20
Q

What is another name for long chain fatty acids?

A

NEFAs

21
Q

How are NEFAs useful in blood work?

A

Good indicator of how much fat is being mobilised

Most fat after a MEAL is carried in the blood as chylomicrons or phospholipid particles whereas mobilised fats are carried as NEFAs

22
Q

How can glycerol be used?

A

Can be used as a gluconeogenic substrate in the liver.

23
Q

What issues need to be resolved when using amino acids as a metabolic intermediate?

How can this be resolved?

A

Need to be deaminated

Produces ammonia

Enters the urea cycle and gets turned into urea

24
Q

How does starvation affect the blood work of omnivores?

A

Increases fat mobilisation

Blood levels of NEFAs UP

25
Q

Where do most NEFAs go when they are created?

What effect can this have?

A

LIVER

Accumulation of FAs in the liver leads to HEPATIC LIPIDOSIS / fatty liver

26
Q

How can you get hepatic lipidosis?

A

Increased fat mobilisation

Increased fat ingestion (more common in humans)

27
Q

How does hepatic lipidosis effect the liver?

A

Impedes flow of blood through sinusoids

Lipid droplets fill cells and marginalise cytosol Therefore reduced intracellular processes

28
Q

How can increased Acetyl CoA (from increased NEFA production) affect the body?

What conditions are associated with this process.

A

Turns on KETOGENESIS and the formation of ketone bodies

Can lead to (diabetic) ketoacidosis, bovine ketosis and twin lamb disease (pregnancy toxaemia

29
Q

How can you test for ketone bodies?

A

Urine

30
Q

What would you expect to see from a cow with ketosis?

A

Slow,
Depressed
Head pressing

31
Q

When are ketone bodies particularly physiologically necessary?

A

Can be converted back into Acetyl co a at target tissue

In BRAIN, can’t use LCFAs as they travel bound to albumin - cant cross BBB

Ketone bodies are short chain FAs and are water soluble - CAN cross BBB as they don’t require carrier molecules

32
Q

Why does Acetyl CoA accumulate?

A

Fat mobilisation

Intermediates taken out of the CAC and converted to glucose therefore less Acetyl CoA used in CAC

33
Q

What VFAs are produced by rumen bacteria?

A

Acetate

Proprionate

Butyrate

34
Q

How are the different VFAs used ?

A

Acetate and Butyrate can be converted into Acetyl CoA or enter the CAC
- Acetyl CoA can be converted into LCFAs which can be used by other tissues or stored in adipocytes as triglycerides

Proprionate can be converted into OAA then converted into glucose via gluconeogenesis

35
Q

What is the major source of blood glucose in ruminants?

A

PROPRIONATE

(-> OOA —> Glucose)

Transported from the liver to the blood

36
Q

What is the normal blood glucose of ruminants?

A

Approximately half the blood glucose of omnivores

2.5 mmol (vs 4.5 mmol)

37
Q

What condition results from high ketone bodies and hypoglycaemia?

What changes would be seen in the blood?

A

Slow cow syndrome

Low glucose
High ketone bodies and NEFAs

38
Q

What might cause a cow to become hypoglycaemic?

A

High production

Twin pregnancies

39
Q

What is primary ketosis?

A

Not taking in enough energy

Negative energy balance

MANY in herd would be affected

40
Q

What is secondary ketosis?

A

Stop taking in food secondary to something else - symptom of another disease

NOT THE ONLY THING THAT IS WRONG

One cow usually affected

41
Q

What conditions can result in secondary ketosis?

A

Laminitis

LDA/RDA

Metritis (retaining foetal membranes)

Mastitis

(Especially around parturition)

42
Q

How are amino acids used in ruminants?

A

Gluconeogenesis - important for preventing ketosis

Microbes can make amino acids out of urea

43
Q

What are the sources of amino acids in ruminants?

A

MICROBIAL PROTEIN (therefore need to make sure microbes are proliferating

Can be supplemented by feeding HEAT TREATED SOY BEAN

44
Q

How is heat treated soy bean a useful element of feed?

A

Not metabolised by microbes therefore goes straight into small intestine where it can be broken down to AMINO ACIDS

(Most amino acids which aren’t protected will be metabolised by the microbes)

BVetMed3 - PMVPH (8 decks)

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