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Endocrine System Brian > The Endocrine Pancreas 1 > Flashcards

The Endocrine Pancreas 1 Flashcards

1
Q

What is meant by the steady state?

A

Body energy = energy intake (food) - energy output

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2
Q

What centres impact the amount of eating?

A

Feeding centre promotes feelings of hunger and drive to eat

Satiety centres promotes feelings of fullness by suppressing the feeding centre

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3
Q

What is activity in both feeding centre and satiety centre controlled by?

A

Complex balance of neural and chemical signals as well as concentration of nutrients in plasma

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4
Q

What are the 2 theories about food intake?

A

Glucostatic theory

Lipostatic theory

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5
Q

What is the glucostatic theory?

A

Food intake determined by blood glucose, as [BG] increases the drive to eat decreases (-feeding centre, +satiety cenre)

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6
Q

What is the lipstatic theory?

A

Food intake determined by fat stores, as fat stores increase the drive to eat decreases (-feeding centre, +satiety centre)

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7
Q

What is a hormone released by fat stores that suppreses the activity of feeding centre?

A

Leptin

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8
Q

What are the 3 categories of energy output?

A

Cellular work

Mechanical work

Heat loss

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9
Q

What are examples of cellular work?

A

Transporting molecules across membranes

Growth and repair

Storage of energy (such as fat, glycogen, ATP synthesis)

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10
Q

What are examples of mechanical work?

A

Movement, either on a large scale using muscles or intracellularly

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11
Q

What is heat loss associated with, and how much of total energy output does in use?

A

Associated with cellular and mechanical work

Accounts for half our energy output

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12
Q

What is metabolism?

A

Integration of all biochemical reactions in the body

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13
Q

What are the 3 elements of metabolism?

A

Extraction energy from nutrients in food

Storing that energy

Utilising that energy for work

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14
Q

What are anabolic pathways?

A

Build up, net effect is synthesis of large molecules from smaller ones, usually for storage purposes

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15
Q

What are catabolic pathways?

A

Breakdown, net effects is degradation of large molecules into small ones, releasing energy for work

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16
Q

What state do we enter after eating?

A

Absorptive state, where ingested nutrients supply the energy needs of the body and excess is stored, this is an anabolic phase

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17
Q

Is the absorptive state an anabolic or catabolic phase?

A

Anabolic phase

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18
Q

What state is entered between meals and overnight?

A

Post-absorptive state (also konwn as fasted state) where we rely on body stores for energy, this is a catabolic phase

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19
Q

Is the post-absorptive phase anabolic or catabolic?

A

Catabolic

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20
Q

The brain is known as an ‘obligatory glucose utiliser’, what does this mean?

A

It has first ‘dibs’ at glucose

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21
Q

What does failure to maintain [BG] in the post-absorptive state lead to?

A

Hypoglycaemia which can lead to coma and death

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22
Q

How is BG maintained during the post-absorptive state?

A

Synthesising glucose from glycogen (glycogenolysis) or amino acids (gluconeogenesis)

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23
Q

What is glycogenolysis?

A

Synthesising glucose from glycogen

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24
Q

What is gluconeogenesis?

A

Synthesising glucose from amino acids

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25
Q

What is the only organ that has access to glucose when it falls below the normal range?

A

The brain

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26
Q

What is the normal range of [BG]?

A

4.2-6.3mM (80-120mg/dL)

5mmoles is useful to remember

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27
Q

What is hypoglycaemia?

A

Plasma glucose concentration falls below 3mM

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28
Q

When does hypoglycaemia occur?

A

When [BG] falls below 3mM

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29
Q

What 2 hormones are key to [BG] being maintained over a fairly tight range?

A

Insulin and glucagon

30
Q

What percentage of the pancreas operates as an exocrine gland?

31
Q

Where does the endocrine function of the pancreas occur?

A

Islets of Langerhans

32
Q

What are the 4 cells present in Islets of Langerhans?

A

Alpha cells

Beta cells

Delta cells

F cells

33
Q

What do alpha cells produce?

34
Q

What do beta cells produce?

35
Q

What do delta cells produce?

A

Somatostatin

36
Q

What do F cells produce?

A

Pancreatic polypeptide

37
Q

Is insulin an anabolic or catabolic hormone?

38
Q

Is glucagon an anabolic or catabolic hormone?

39
Q

What effects does insulin have that makes it an anabolic hormone?

A

Increased glucose oxidation

Increased glycogen synthesis

Increased fat synthesis

Increased protein synthesis

40
Q

What effects does glucagon have that makes it a cataboic hormone?

A

Increases glycogenolysis

INcreases gluconeogenesis

Increases ketogenesis

41
Q

What class of hormone is insulin?

A

Peptide hormone

42
Q

What does insulin do?

A

Stimulates glucose uptake by cells

43
Q

Explain the process of insulin production?

A

1) Synthesised as large preprohormone by ribosomes (called preproinsulin) which is converted to proinsulin in ER
2) Proinsulin packaged as granules in secretory vesicles, within grandules it is cleaved again to give insulin and C-peptide
3) Insulin stored in this form until B cell is activated and secretion occurs

44
Q

How is insulin secretion stimulated during the absorptive phase?

A

Both glucose and amino acids stimulate insulin secretion, but major stimulus is blood glucose concentration

45
Q

Other than insulin, do any other hormones lower [BG]?

A

No, only insulin lowers blood glucose concentration

46
Q

During the absorptive state, what is excess glucose stored as?

A

Glycogen in liver and muscles and as triacylglycerols (TAG) in the liver and adipose tissue

47
Q

During the absorptive state, what are excess amino acids used for?

A

To make new proteins with excess being converted to fat, also a form of energy

48
Q

In the absorptive state, what are fatty acids stored as?

A

Triglycerides in adipose tissue and liver

49
Q

Explain the mechanism of control of insulin secretion by [BG]?

A

1) B cells have specific type of K channel that is sensitive to [ATP] within the cell (called a KATP channel)
2) When glucose is abundent enters through glucose transporter protein (GLUT) and metabolism increases, increasing [ATP] within cell and causing KATP channel to close
3) Causes intracellular K to rise, repolarising the cell
4) Voltage dependent calcium channels open and trigger insulin vescicle exocytosis into the circulation

50
Q

Explain the mechanism of KATP channels in the pancreas when [BG] is low?

A

1) ATP concentration is low so KATP channels are open so K flows out removing the plus charge from the cell and hyperpolarising it
2) Voltage gated calcium channels remain closed and insulin is not secreted

51
Q

What receptor does insulin bind to?

A

Tyrosine kinase receptors on cell membrane of insulin-sensitive tissues to increase glucose uptake by those tissues

52
Q

What does insulin stimulate in muscle and adipose tissue?

A

Mobilisation of specific glucose transporters (GLUT-4) which resides in the cytoplasm of these cells

53
Q

What does GLUT-4 do when stimulated by insulin?

A

Migrates to cell membrane and transports glucose into cell, when insulin stops GLUT-4 transporters return to cytoplasm

54
Q

What do tyrosine kinases always do?

A

Phosphorylate other proteins as part of their signal transduction

55
Q

Do all tissues require insulin to take up glucose?

A

No, most tissues do not - only muscle and fat are insulin dependent

However, muscle and fat take up a large proportion of the body

56
Q

What percentage of body weight is muscle?

57
Q

What percentage of body weight is fat?

A

About 20-25% (in healthy individual)

58
Q

What are examples of glucose transports that tissues use that are not insulin dependent?

A

GLUT1

GLUT2

GLUT3

59
Q

What are some tissues that use GLUT 1 transporters?

A

Brain, kidney, red blood cells

60
Q

What uses GLUT-2 transporters?

A

B cells of pancreas and liver

61
Q

What are examples of tissues that use GLUT-3 transporters?

A

Similar to GLUT1: brain, kidney, red blood cells

62
Q

How do GLUT tranporters that are not insulin dependent allow glucose to enter cells?

A

Down concentration gradient

63
Q

How does insulin affect entry of glucose into hepatocytes?

A

Has no direct effect (as GLUT-2 transporters are used in liver)

But insulin allows more glucose to enter due to causing the metabolism of glucose inside hepatocytes to keep the intracellular concentration low and maintain concentration gradient

64
Q

What are some additional actions of insulin?

A
  • Increases glycogen synthesis in muscle and liver, stimulates glycogen synthase and inhibits glycogen phosphorylase
  • Increases amino acid uptake into muscle, promoting protein synthesis
  • Increases protein synthesis and inhibits proteolysis
  • Increases triacylglycerol synthesis in adipocytes and liver, ie, stimulates lipogenesis and inhibits lipolysis
  • Inhibits the enzymes of gluconeogenesis in the liver
  • Promotes K+ ion entry into cells by stimulating Na+/K+ ATPase, very important clinically
65
Q

How can insulin have many different actions?

A

Possible because of multiple signal transduction pathways associated with insulin receptor

66
Q

What is the half life of insulin?

A

About 5 minutes

67
Q

Where is insulin principally degraded?

A

Liver and kidneys

68
Q

What happens to insulin bound receptors once their action is done?

A

Internalised by endocytosis and destroyed by intulin protease, some is recycled

69
Q

What are some examples of stimuli that increases insulin release?

A
  • Increased [BG]
  • Increased [amino acids]plasma
  • Glucagon (insulin required to take up glucose created via gluconeogenesis stimulated by glucagon)
  • Other (incretin) hormones controlling GI secretion and motility
    • Such as gastrin, secretin, CCK, GLP-1, GIP
    • Released by ileum and jejunum in response to nutrients, early insulin prevents glucose surge when absorption occurs
  • Vagal nerve activity
70
Q

What are examples of incretin hormones controlling GI secretion and motility that stimulate insulin release?

A

Gastrin, secretin, CCK, GLP-1, GIP

Released by ileum and jejenum in response to nutrients, early insulin prevents glucose surge when absorption occurs

71
Q

What are examples of stimuli that inhibit insulin release?

A

Low [BG]

Somatostatin (GHIH)

Sympathetic alpha2 effects

Stress (such as hypoxia)

72
Q

Why is the insulin response to an IV glucose load less than the equivalent amount of glucose administered orally?

A

IV glucose causes increase in insulin by direct effect of increased glucose on beta cells

Oral loading of same amount causes increased insulin by both direct effect on beta cells and vagal stimulation of beta cells, plus incretin effects

Endocrine System Brian (26 decks)

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