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PoM > MBC - Integration of Metabolism > Flashcards

MBC - Integration of Metabolism Flashcards

1
Q

What does the muscle use for ATP supply during light contraction?

A

Relies on oxidative phosphorylation

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2
Q

What does the muscle do when contraction becomes more vigorous?

A

Relies on the breakdown of glycogen stores

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3
Q

What is broken down during anaerobic conditions?

A

pyruvate is broken down into lactate via LDH

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4
Q

Where does lactate go once produced in muscles?

A

the liver

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5
Q

What does the brain constantly require?

A

Glucose

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6
Q

What can the brain not metabolise?

A

Fatty acids

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7
Q

What can partially substitute for glucose in the brain?

A

Ketone bodies

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8
Q

What is caused by hypoglycaemia?

A

Faintness/coma

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9
Q

What is caused by hyperglycaemia?

A

Irreversible damage especially to nerve rich cells such as the retina.

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10
Q

What are myocytes designed for?

A

Aerobic respiration

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11
Q

How are myocytes ideal for aerobic respiration?

A

Rich in mitochondria Utilise TCA substrates such as free fatty acids and ketone bodies.

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12
Q

What happens when energy demand in the heart exceeds energy supply?

A

Loss of oxygen leads to cell death and myocardial infarction

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13
Q

What is the role of the liver?

A

Highly metabolically active: - interconverts nutrient types - central role in maintaining blood glucose levels - stores glucose as glycogen - Lipoprotein metabolism - key in triglyceride/cholesterol transport

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14
Q

What is the level of glucose that the liver tries to maintain?

A

4.0-5.5 mM

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15
Q

What is the first step of carbohydrate metabolism?

A

Carbohydrate is tier broken down into glucose or other simple sugars

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16
Q

What happens to glucose after being formed by carbohydrates?

A

It is broken down into glucose-6-phosphate via hexokinase

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17
Q

What happens to simple sugars after being formed from carbohydrates?

A

they are converted to glucose-6-phosphate

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18
Q

What happens to glucose-6-phosphate?

A

Either becomes pyruvate. Excess glucose-6-phosphate will become glycogen, or it can enter pentose phosphate pathway to generate nucleotides, and NADPH for anabolic reactions e.g. cholesterol synthesis

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19
Q

What happens to pyruvate?

A

Can either become acetyl-CoA, or backbone can be used for amino acids to become nucleotides, or can become lactate in anaerobic conditions.

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20
Q

What happens to acetyl-CoA?

A

Can enter TCA cycle, or can become fatty acids/cholesterol if in excess, or ketone bodies in conditions of starvation.

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21
Q

What happens in the TCA cycle?

A

Oxidation of small molecules and subsequent oxidative phosphorylation, or some products can become amino acids and subsequently nucleotides.

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22
Q

How does the body avoid hypoglycaemia in the short term?

A

Breakdown of glycogen stores Release of free fatty acids from adipose tissue Convert acetyl-CoA to ketone bodies in the liver

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23
Q

How long can the body resist hypoglycaemia for?

A

12-18 hours

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24
Q

What does the body do after 12-18 hours of resisting hypoglycaemia?

A

Uses gluconeogenesis to generate glucose form pyruvate/oxaloacetate

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25
Q

What is the first step of gluconeogenesis?

A

Pyruvate is converted to oxaloacetate via pyruvate carboxylase

26
Q

Where does the conversion of pyruvate to oxaloacetate occur?

A

Mitochondria

27
Q

Where does gluconeogenesis primarily occur?

A

Cytoplasm

28
Q

What are the irreversible reactions from glycolysis and how do we bypass them?

A

Reactions involving kinases from glycolysis We bypass them by using phosphatases

29
Q

What is the second step of gluconeogenesis?

A

Oxaloacetate is converted to phosphoneolpyruvate via phosphoenolpyruvate carboxykinase

30
Q

What is the third step of gluconeogenesis?

A

Phosphoenolpyruvate is converted to fructose-1,6-bisphosphate

31
Q

What is the fourth step of gluconeogenesis?

A

fructose-1,6-bisphosphate is converted to fructose-6-phosphate via fructose-1,6-bisphosphatase.

32
Q

What is the fifth step of gluconeogenesis?

A

Fructose-6-phosphate is converted to glucose-6-phosphate

33
Q

What is the sixth and final step of gluconeogenesis?

A

Glucose-6-phosphate is converted to glucose via glucose-6-phosphatase.

34
Q

At what level of glucose is a hypoglycaemic coma induced?

A

Below 3mM of glucose.

35
Q

How do proteins contribute to gluconeogenesis?

A

Degradation of all 20 amino acids leads to 7 products. Glucogenic amino acids have skeletons which give rise to glucose via gluconeogenesis.

36
Q

How do proteins contribute to fatty acid/ketone body formation?

A

Ketogenic amino acids have skeletons which can be used for fatty acid synthesis or ketogenesis.

37
Q

How do fatty acids contribute to glucose metabolism?

A

Can’t be converted into glucose however can be converted into ketone bodies thus metabolised by tissues e.g. muscle and brain.

38
Q

How does glycerol contribute to glucose metabolism?

A

Glycerol can be converted into DHAP which can be used in the gluconeogenic pathway upstream.

39
Q

What is typically the main focus for controlling metabolic reactions?

A

Irreversible reactions

40
Q

When is the greatest level of control achieved? Give an example

A

Greatest level of control is achieved when control steps e.g. inhibition, are placed early in the downstream pathway. For example, hexokinase is inhibited easily by G-6-P, therefore in anaerobic conditions, G-6-P builds up and hexokinase is inhibited early.

41
Q

What happens in aerobic exercise?

A

Contractions increase ATP demand Contractions increase glucose transport into muscle

42
Q

How does the body respond to aerobic exercise?

A

Increase in glucose transporters in myocyte membranes. Adrenalin increases muscle glycolysis Adrenalin increases fatty acid release from adipocytes Adrenalin increases gluconeogenesis in the liver.

43
Q

What happens in anaerobic exercise?

A

ATP demand cannot be matched by O2 delivery Glucose transport (supply) cannot match demand

44
Q

How does the body respond to anaerobic exercise?

A

Muscle glycogenolysis increases Pyruvate is broken down into lactate + H+. Liver then uses lactate to form pyruvate and thus generate glucose via gluconeogenesis (pyruvate to lactate is a reversible reaction with the oxidation of NADH to NAD+)

45
Q

What can control steps be in the form of?

A

Product inhibition Signal influence e.g. hormones

46
Q

What is Michaelis constant (Km)?

A

The concentration at which an enzyme functions at half of its maximal rate (half of Vmax)

47
Q

Explain the difference in hexokinase Km between liver and muscle

A

There are different hexokinase isoforms in the liver and muscle. In the muscle, HK1 has Km of 0.1mM whereas in the liver, HKIV has Km of 4.0mM.

48
Q

Explain the significance of a low Km in muscle.

A

This means that hexokinase in the muscle undergoes glycolysis readily as it is sensitive to glucose. It is also inhibited easily by G-6-P due to its high sensitivity.

49
Q

Explain the significance of a high Km in the liver.

A

This means that hexokinase IV is less active and less sensitive to glucose levels and G-6-P levels, therefore less easily inhibited.

50
Q

What enzyme is present in the liver but not the muscle?

A

Glucose-6-phosphatase (for gluconeogenesis)

51
Q

What is the role of insulin?

A

Reduces blood sugar levels: - Increases glucose uptake by liver and cells - Increases synthesis of fats and proteins - Increases storage of glucose as glycogen and fat.

52
Q

What is the role of glucagon?

A

Increases blood sugar levels: - Increases HGO - Increases lipolysis and ketogenesis - Increases glycogenolysis

53
Q

What is the role of adrenalin?

A

Rapidly mobilises glucose for a fight or flight response

54
Q

What is the role of glucocorticoids?

A

Steroid hormones that increase the synthesis of enzymes concerned with glucose availability.

55
Q

What happens on having a meal to hormone levels?

A

Insulin rises to counteract the quick rise in glucose in the blood, glucagon falls. - Increased glucose uptake by liver and muscle for glycogen synthesis. - Increased glycolysis by liver (acetyl CoA is used for fatty acid synthesis). - Increased triglyceride synthesis in adipose tissue - Increased usage of metabolic intermediates due to general stimulatory effect and growth.

56
Q

What happens after having a meal?

A

Glucose levels start to fall so is controlled by: - Increased glucagon and reduced insulin for islets. - HGO increases from glycogen breakdown and gluconeogenesis - Lipolysis used as alternative substrate for ATP production. - Similar effects to adrenalin

57
Q

What are the effects of adrenalin?

A

Similar to that of glucagon, but adrenalin also stimulates glycolysis and glycogen breakdown in skeletal muscle, and lipolysis in adipose tissue.

58
Q

What happens during prolonged fasting to the glucagon:insulin ratio?

A

increases further

59
Q

What happens during prolonged fasting to adipose tissue?

A

Lipolysis increases for metabolism

60
Q

What happens during prolonged fasting to the TCA cycle?

A

Intermediates for TCA are reduced to provide substrates for gluconeogenesis.

61
Q

What happens during prolonged fasting to proteins?

A

Proteolysis increases to provide amino acid substrates for gluconeogenesis

62
Q

What happens during prolonged fasting to ketone bodies?

A

Ketogenesis arises from fatty acids and amino acids to partially substitute for glucose in the brain.

PoM (27 decks)

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