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Physiology 1 > Endocrine Control Of Metabolism > Flashcards

Endocrine Control Of Metabolism Flashcards

1
Q

What are the circulating nutrients that are affected by hormones?

A

Glucose, fatty acids, amino acids, ketone bodies, lactate

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2
Q

What are the stored nutrients that are affected by hormones?

A

Glycogen, triglycerides and body proteins

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3
Q

What is the normal plasma glucose concentration?

A

5 mmol/L

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4
Q

What is the critical plasma glucose level?

A

<2.5 mmol/L

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5
Q

What happens in hypoglycaemia?

A

Coma and death

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6
Q

What happens in hyperglycaemia?

A

Chronic exposure to increase glucose concentrations -> protein damage via non-enzymatic glycation

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7
Q

What are the two phases of metabolism?

A

Absorptive and fasting

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8
Q

What hormones are involved in the absorptive stage of metabolism?

A

Insulin

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9
Q

What hormones are involved in the fasting stage of metabolism?

A

Glucagon, adrenaline, cortisol and GH

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10
Q

What are the two main effects of insulin?

A

Stimulates nutrient storage and inhibits nutrient release

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11
Q

What are the ways in which insulin stimulates nutrient storage?

A
  • Uptake of glucose by skeletal muscle, adipose and other tissues
  • glycogen synthesis in liver, skeletal muscle
  • uptake of fatty acids and amino acids
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12
Q

How does insulin inhibit nutrient release?

A

Inhibits release of glucose from liver (hepatic glucose production)
Inhibits fat and protein breakdown (lipolysis and proteolysis)

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13
Q

What does glucagon stimulate?

A

Hepatic glucose production

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14
Q

What does adrenaline do?

A

Stimulates hepatic glucose production and stimulates lipolysis

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15
Q

What is lipolysis?

A

Fatty acid release from adipose tissue stores

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16
Q

What does GH stimulate?

A

Hepatic glucose production and lipolysis

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17
Q

What does cortisol do?

A

Stimulates hepatic glucose production and lipolysis and proteolysis

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18
Q

What are the three metabolic pathways that serve energy storage?

A

Glycogenesis, lipogenesis and triglyceride synthesis

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19
Q

What is triglyceride synthesis?

A

Esterification of fatty acids for storage as triglycerides

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20
Q

What are the metabolic pathways serving energy release?

A

Glycogenolysis, glycogenesis, lipolysis, beta oxidation and ketogenesis

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21
Q

What is ketogenesis?

A

Production of ketone bodies from acetyl coA

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22
Q

What is beta oxidation?

A

Fatty acids -> acetyl coA

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23
Q

What is lipolysis?

A

Release of fatty acids from triglyceride breakdown

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24
Q

What is gluconeogenesis?

A

Synthesis of glucose from non-carb substances

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25
Q

What does glucagon stimulate?

A

Glycogenolysis and gluconeogenesis

26
Q

What hormones stimulates lipolysis?

A

Adrenaline and GH

27
Q

What is a decrease in plasma glucose sensed by?

A

Pancreatic islet cells and CNS

28
Q

What do the pancreatic islet cells do if plasma glucose levels decrease?

A

Alpha cells secrete glucagon to increase glucose production

29
Q

What happens when the the CNS senses plasma glucose decrease?

A

Increase sympathetic flow to the liver, pancreas and chromaffin cells

30
Q

What do chromaffin cells do when activated?

A

Release adrenaline that stimulates pancreatic alpha cells and liver

31
Q

What are the short term defences against hypoglycaemia?

A

Glucagon, adrenaline and SNS

32
Q

What are the medium term defences against hypoglycaemia?

A

Ketogenesis

33
Q

What are the long term defences against hypoglycaemia?

A

Cortisol stimulates proteolysis to supply amino acid substrates for gluconeogenesis

34
Q

What are the defences against hyperglycaemia?

A

Insulin

35
Q

How does insulin defend against hyperglycaemia?

A

Stimulates glucose uptake by tissues and inhibits hepatic glucose production

36
Q

What is type 1 diabetes mellitus?

A

Complete insulin deficiency

37
Q

What is type 2 diabetes mellitus?

A

Insulin insufficiency combined with resistance

38
Q

What are the main insulin sensitive tissues in the body?

A

Liver, skeletal muscle and adipose tissue

39
Q

Why is the liver insulin sensitive?

A

Maintains [plasma glucose]

40
Q

Why is skeletal muscle insulin sensitive?

A

Buffers rise in [plasma glucose]

41
Q

Why is adipose tissue insulin sensitive?

A

Store dietary fats/ excess glycogen

42
Q

What’s special about adipocytes?

A

They have a large fat droplet that occupies most of the cell volume

43
Q

How do TGs enter a cell?

A

Broken down into fatty acids by lipoprotein lipase and then re-Esterified once inside the adipocyte

44
Q

How are TGs transported?

A

Either as chylomicrons or VLDLs

45
Q

What is lipoprotein lipase stimulated by?

A

Insulin

46
Q

What is GLUT4 dependant on?

A

Insulin

47
Q

What is hormone sensitive lipase stimulated by?

A

Adrenaline and noradrenaline

48
Q

What enzymes break down stored TGs?

A

Hormone sensitive lipase

49
Q

What is glycerol used for in the liver?

A

Gluconeogenesis

50
Q

What processes break down fatty acids?

A

Beta oxidation or ketogenesis

51
Q

How can glucose be taken up in muscle?

A

GLUT4 receptors or muscle contraction

52
Q

When are fatty acids used for energy in muscle?

A

Endurance exercise

53
Q

Where is glucose metabolism directed with high insulin and low glucagon?

A

Towards glycogen storage

54
Q

Where are amino acids directed with low insulin and high glucagon?

A

Away from protein synthesis and into glyconeogenesis

55
Q

Where can acetyl CoA be used?

A

TCA cycle or ketogenesis

56
Q

What is malonyl CoA?

A

First intermediary in lipogenesis

57
Q

What does malonyl coA inhibit (and how)?

A

Fatty acyl coA -> keto acids

Blocking the movement of fatty acyl CoA into mitochondria by blocking CPT (a transporter)

58
Q

What can ketone bodies cause at high concentrations?

A

Acidosis

59
Q

What is ketone body-induced acidosis usually buffered by?

A

HCO3-

60
Q

How does diabetic ketoacidosis happen?

A

In the absence of insulin, gluconeogenesis, lipolysis and beta oxidation are unregulated so increase

61
Q

What happens if gluconeogenesis, lipolysis and beta oxidation is unregulated?

A

Oxaloacetate from TCA cycle being used up in gluconeogenesis so not combined with acetyl CoA and so acetyl CoA builds up

62
Q

What happens to the built up acetyl coA when there’s no insulin present?

A

Funnelled into ketogenesis and increase in [acetate] and [hydroxybutyrate]

Physiology 1 (65 decks)

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