Integration Of Metabolism Flashcards

1
Q

Muscle

A

Relies upon carbohydrate and fatty acid oxidation

Have periods of very high ATP requirement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Brain and nervous system

A

Cannot utilise fatty acids as a fuel source

Uses 20% of resting metabolic rate —> has continuous high ATP requirement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Adipose tissue

A

Long term storage site for triglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Heart

A

Can oxidise fatty acids and carbohydrates

10% of resting metabolic rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Liver

A

Main carbohydrate store

Source of blood glucose

20% resting metabolic rate

Source of ketone bodies (from fatty acids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does the brain require a continuous supply of?

A

Glucose

(Ketone bodies can partially substitute for glucose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can the brain not metabolise?

A

Fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In the brain what does too little and too much glucose cause?

A

Too little = hypoglycaemia —> fairness and coma

Too much = hyperglycaemia —> irreversible damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In the muscle how are requirements met during light contraction?

A

OxPhos
—> O2 and blood borne glucose and fatty acids used as fuel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In the muscles how are requirements met during vigorous contraction?

A

Glycogen breakdown

Lactate formation

When ATP consumption > than ATP supply rate by OxPhos
—> O2 becomes a limiting factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Metabolic features of the heart

A

Completely aerobic metabolism —> rich in mitochondria

Utilises TCA substrates —> free fatty acids, ketone bodies e.g.

Loss of O2 —> cell death —> myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens during extreme exercise?

A

ATP demand > ATP production
—> lactate produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens during fasting?

A

Instead of entering TCA cycle —> acetyl CoA results in ketone body production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens if glucose levels fall below 3 mM?

A

Body enters a hypoglycaemic coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is hypoglycaemia avoided?

A

Breakdown of liver glycogen stores —> maintain plasma glucose levels

Release free fatty acids from adipose tissue

Convert acetyl CoA into ketone bodies via the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What reaction can directly enter pathway to increase oxaloacetate for gluconeogenisis?

A

Transamination of amino acids
—> carbon skeleton enters the cycle

17
Q

Why must some redactions on gluconeogenisis be bypassed?

A

The forward reactions are essentially irreversible under cellular conditions

18
Q

Why can’t the muscle produce glucose via gluconeogenisis?

A

It doesn’t have the enzyme (glucose-6-phosphatase) to bypass the reaction

19
Q

Why is it important that the muscle doesn’t have glucose-6-phosphatase?

A

It ill reverse the reaction —> set up a futile cycle

20
Q

What are glucogenic amino acids used for?

A

Generate glucose via gluconeogenisis

21
Q

What are ketogenic amino acids used for?

A

Synthesis fatty acids and ketone bodies

22
Q

Fats as a fuel source

A

Triglycerides —> fatty acids and glycerol

Fatty acid —> ketone bodies

Glycerol —> DHAP —> enter gluconeogenisis

23
Q

Energy stores and consumption - Aerobic respiration

A

Contractions increase ATP demand

Contractions increase glucose transport

Muscle glycolysis increases (adrenalin)

Gluconeogenisis increases (adrenalin)

Fatty acids increase (adrenalin)

24
Q

Energy stores and consumptions - Anaerobic respiration

A

ATP demand not matched by O22 delivery

Transport cannot keep up with the demand for glucose

Muscle glycogen breakdown increases

Lactate increases

Liver uses lactate to form glucose (recovery) —> replenishes NAD+ levels

25
Q

Hormonal control of blood - what does insulin do?

A

Secreted by islets of pancreas when glucose levels rise

Stimulate uptake and use of glucose and storage of glycogen and fat

Suppresses glucagon release

26
Q

Hormonal control of blood — what does glucagon do?

A

Secreted by islet of pancreas when glucose levels fall

Stimulates production of glucose by gluconeogenisis and breakdown of glycogen and fat

27
Q

Hormonal control of blood - what does adrenalin do?

A

Strong and fast metabolic effects to mobilise glucose for ‘fight or flight’

28
Q

Hormonal control of blood - what do glucocorticoids do?

A

Steroid hormones —> increases synthesis of metabolic enzymes concerned with g;leucose availability

29
Q

Hormonal control of blood - right after a meal

A

Blood glucose levels rise —> controlled by increased secretion of insulin and reduced glucagon

Increased glucose uptake by liver

Increased glucose uptake and glycogen synthesis in muscle

Increased triglyceride synthesis in adipose tissue

Increased usage of metabolic intermediates

30
Q

Hormonal control of blood - some time after a meal

A

Blood glucose levels start to fall and are controlled by:

Increased glucagon secretion + reduced insulin

Glucose production in liver from glycogen breakdown and gluconeogenisis

Fatty acid breakdown as alternative substrate for ATP production

Adrenalin stimulera glycogen breakdown, glycolysis + lipolyses

31
Q

Hormonal control of blood - after prolonged fasting

A

Glucagon/insulin ratio increases further

Adipose tissue hydrolyses triglycerides to provide fatty acids

TCA cycle intermediates reduced in amount to provide substrates for gluconeogenisis

Protein breakdown provides amino acid substrates for gluconeogenisis

Ketone bodies produced from fatty acids and amino acids in liver

32
Q

Type 1 diabetes

A

Failure to secret enough insulin (beta cell dysfunction)

33
Q

Type 2 diabetes

A

Failure to respond appropriately to insulin levels (insulin resistance)

34
Q

What are some complications of diabetes?

A

Hyper and hypoglycaemia

Cardiovascular complications

Ketoacidosis