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Endo: Sem 2 > Control of Metabolism > Flashcards

Control of Metabolism Flashcards

1
Q

What are the two methods of ATP generation?

A
  1. Glycolysis of glucose into pyruvate (net yield of 2 ATP) anaerobically
  2. Acetyl CoA in Krebs cycle converted into 30+ ATP molecules aerobically
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2
Q

What in the Krebs cycle drives the production of ATP?

A

Electron Transport Chain

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3
Q

What types of molecules can be used in the Krebs cycle to drive ATP production?

A

Carbohydrates, Fats, Amino Acids

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4
Q

How are fatty acids broken down into Acetyl CoA?

A

Via β-oxidation

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5
Q

What happens to excess glucose and why?

A

It is stored as glycogen for release between meals

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6
Q

What are the circulating nutrients?

A

Glucose, fatty acids, amino acids, keto bodies, lactate

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7
Q

What are the stored nutrients?

A

Glycogen, triglycerides, body proteins

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8
Q

What is the normal plasma glucose concentration?

A

5 mmol L-1

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9
Q

What is hypoglycaemia?

A

Low blood glucose can lead to coma and death

< 2.5 mmol L-1 is critically low

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10
Q

What is hyperglycaemia?

A

Very raised blood glucose leading to protein damage and non-enzymatic glycation

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11
Q

How much glucose can we gain from our food per day?

A

3000 mmol day-1

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12
Q

What are the two metabolic states?

A

o Absorptive

o Fasting

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13
Q

What occurs during the absorptive state?

A

Nutrients are being absorbed from the gut and entering circulation

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14
Q

What occurs during the fasting state?

A

There are no nutrients to absorb from the gut and we live off stored nutrients

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15
Q

Which hormones regulate the switch between these two states to maintain blood sugar levels?

A

Insulin: dominates absorptive state
 Released as blood glucose rises and promotes storage of glycogen
Glucagon: dominates post-absorptive state
 Causes nutrient release to raise blood glucose levels after they drop
Cortisol, growth hormone (somatotropin),
Adrenaline: releases nutrients raising blood sugar levels

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16
Q

Which four tissues does insulin promote the uptake of glucose in?

A
  1. Adipose Tissue (fat)
  2. Skeletal Muscle
  3. Cardiac Muscle
  4. Liver
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17
Q

Which processes does insulin inhibit?

A

Gluconeogenesis, glycogenolysis, lipolysis, proteolysis

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18
Q

What are the different metabolic pathways?

A 
1. Glycogenolysis:
Release of glucose from glycogen stores
2. Gluconeogenesis:
De novo synthesis of glucose from non-carbohydrate substances
3. Lipolysis:
Release of fatty acids from TG breakdown
4. β-oxidation:
Fatty acids to Acetyl CoA
5. Ketogenesis
Production of ketone bodies from Acetyl CoA
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19
Q

What effect does insulin have on free fatty acids and amino acids?

A

Promotes uptake into adipose tissue and muscle tissue

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20
Q

What are the short-term defences against hypoglycaemia?

A

o Glucagon
o Epinephrine
o Sympathetic NS

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21
Q

What about medium and long term defences against hypoglycaemia?

A

o Ketogenesis: fat reserves can provide a partial substitute for glucose, sparing muscle tissue from destruction that would otherwise be needed to provide amino acid substrates for gluconeogenesis
o Cortisol promotes proteolysis to supply amino acids

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22
Q

What are the major effects of glucagon?

A

Stimulates hepatic glucose production in the liver

23
Q

What are the major effects of adrenaline (and sympathetic NS)?

A

o Stimulates hepatic glucose production

o Stimulates lipolysis: release of FA from adipose tissue

24
Q

What are the major effects of growth hormone?

A

Stimulates hepatic glucose production and lipolysis

25
Q

What are the defences against hyperglycaemia?

A

Insulin which stimulates glucose uptake by tissues and inhibits hepatic glucose production

26
Q

What does lack of insulin action lead to?

A

Hyperglaecemia and diabetes mellitus

27
Q

What is the difference between type I and type II diabetes mellitus?

A

o Type I is insulin deficiency

o Type II is insulin insufficiency combined with insulin resistance

28
Q

In the absorptive state, how does blood glucose rise in the cells?

A

o Glucose enters cells via GLUT protein channels (expression stimulated by insulin)
o It is immediately phosphorylated to maintain diffusion gradient so glucose keeps entering cell

29
Q

Is glucagon an agonist or antagonistic hormone?

A

Antagonist

o Causes nutrient releasing pathways to stop blood glucose falling too slow when it is released.

30
Q

Give an example of gluconeogenesis?

A

o Amino acids being converted to glucose via pyruvate

o Synthesis of glucose from a non-carbohydrate compound

31
Q

Why is blood glucose maintenance important?

A

o The brain is entirely dependent on aerobic metabolism and doesn’t have ability to oxidise fatty acids
o Needs constant uninterrupted supply of glucose via circulation

32
Q

What does insulin cause in the liver?

A

o Glycogenesis
o Glycolysis
o Lipogenesis

33
Q

What does insulin cause in the muscle?

A

o Glucose uptake
o Amino acid uptake
o Glycogenesis

34
Q

What does insulin cause in the adipose tissue?

A

o Glucose uptake
o Free fatty acid uptake
o Lipogenesis

35
Q

What does glucagon cause in the liver?

A

o Glycogenolysis
o Gluconeogenesis
o Ketogenesis

36
Q

What GLUT transporter is responsible for glucose uptake in muscle?

A

o GLUT4 stimulated by insulin

o Increase their expression on cell membrane to increase glucose permeability

37
Q

How else does insulin effect the muscles?

A

o Stimulates amino acid uptake

o Stimulates glycogenesis

38
Q

What is the function of white adipose tissue?

A

o Synthesis of TAG from fatty acids and glucose
o Release fatty acids from storage
o Fatty acids are transported to tissues in lipoproteins

39
Q

How does insulin effect the white adipose tissue?

A

o Stimulates glucose uptake via GLUT 4 transporters
o Stimulates FA uptake by stimulating lipoprotein lipase
o Lipogenesis

40
Q

Why are lipids transported as lipoproteins?

A

They are insoluble in water

41
Q

What are chylomicrons?

A

o They carry absorbed fat from the gut to liver/adipose tissue
o Only present in absorptive state

42
Q

What enzyme breaks down TAGs?

A

Lipoprotein lipase

43
Q

What happens to fatty acids after being taken up by adipocytes?

A

Converted to TAGs and stored for release later

44
Q

What are VLDL?

A

o Some of the chylomicrons pass by liver and the FAs get released as VLDLs
o Very-low-density-lipoprotein supplying blood with fatty acids
o In fasting state, TAGs transported in the VLDL particles so that FA released at tissues

45
Q

What methods of glucose metabolism occur in the liver?

A

Glycogen formation, glycogenolysis, gluconeogenesis

46
Q

What about amino acid formation?

A

Lipogenesis, ketogenesis, gluconeogenesis

47
Q

What about fatty acid metabolism?

A

o Lipogenesis

o Ketogenesis

48
Q

Why are gluconeogenesis and fatty acid oxidation in competition in the liver?

A

Both require oxaloacetate
 Oxidation of Acetyl CoA to enter Krebs cycle
 Oxaloacetate to phosphoenol pyruvate for gluconeogenesis

49
Q

How do we get around a build-up of ACoA if oxaloacetate gets used for gluconeogenesis instead?

A

o ACoA is metabolised into ketone bodies (acetoacetate, 3-hydroxybutyrate and acetone) so less amino acid demand so less protein breakdown
o Ketone bodies enter circulation and used in muscles where its reconverted into AcoA and enters krebs to produce ATP
o Used in times of starvation and when limited glucose is being conserved.

50
Q

Why does the body think its starving in type I diabetes?

A

o No insulin released (dominant in absorptive state) so no indication of absorptive state
o Lack of insulin

51
Q

Why does diabetic ketoacidosis occur?

A

o Ketone bodies build up because lots of gluconeogenesis occurs (due to lack of insulin) meaning there is lots of ACoA that undergo ketogenesis
o Ketone bodies are mildly acidic and the blood doesn’t have enough buffering as it gets overwhelmed so you get diabetic ketoacidosis

52
Q

How does diabetes all start?

A

o Begin hyperglycaemic as glucose absorbed from gut isn’t taken up by the tissues (no insulin)
o Body making more glucose via gluconeogenesis as not inhibited by insulin = raised blood sugar
o Causes osmotic problems and glycosuria

53
Q

What is glycosuria?

A

o Glucose in urea as glucose filtrated from blood into tubule instead of being reabsorbed
o Causes osmotic diuresis as high osmolarity in tubule = less water reabsorption = dehydration = thirsty
o Impairs kidneys as won’t be as good excreting H+ so = acidosis = ketoacidosis

Endo: Sem 2 (11 decks)

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