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*Diabetes & Endocrinology > Endocrine Pancreas 1 > Flashcards

Endocrine Pancreas 1 Flashcards

1
Q

Body energy =

A

energy intake - energy ouput

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2
Q

Energy (food) intake is determined by balance of activity of which 2 hypothalamic centres?

A

Feeding centre

Satiety centre

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3
Q

What is the function of the feeding centre?

A

Promotes feelings of hunger and drive to eat

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4
Q

What is the function of the satiety centre?

A

Promotes feelings of fullness by suppressing the feeding centre

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5
Q

What is the glucostatic theory?

A

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

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6
Q

What is the lipostatic theory?

A

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

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7
Q

What part does leptin play in the lipostatic theory?

A

Leptin is a peptide hormone released by fat stores which depresses feeding activity (not the only signal in the system, as obesity proves…)

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8
Q

What can result from disruption of these pathways?

A

Obesity

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9
Q

What are the 3 categories of energy output?

A

Cellular work
Mechanical work
Heat loss

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10
Q

Describe cellular work

A

transporting molecules across membranes; growth + repair; storage of energy (e.g. fat, glycogen, ATP synthesis)

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11
Q

Describe mechanical work

A

movement, either on large scale using muscle or intracellularly

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12
Q

Describe heat loss

A

associated with cellular and mechanical work - accounts for half of our energy output

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13
Q

What is the only part of energy output we can regulate voluntarily?

A

Mechanical work

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14
Q

What is metabolism?

A

Integration of all biochemical reactions in the body

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15
Q

What are the 3 elements of metabolism?

A
  1. extracting energy from nutrients in food
  2. storing that energy
  3. utilising that energy for work
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16
Q

Describe anabolic pathways

A

‘BUILD UP’

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

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17
Q

Describe catabolic pathways

A

‘BREAK DOWN’

net effect is degradation of large molecules into smaller ones, releasing energy for work

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18
Q

What state do we enter after eating?

A

Absorptive state

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19
Q

Describe the absorptive state

A

state where ingested nutrients supply the energy needs of the body and excess is stored = anabolic

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20
Q

What state do we enter between meals and overnight?

A

Post-absorptive state

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21
Q

Describe the post-absorptive state

A

The pool of nutrients in the plasma decreases and we enter this state where we rely on body stores to provide energy = catabolic

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22
Q

What is the brain described as?

A

‘Obligatory Glucose Utiliser’ !!

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23
Q

What substances can the brain use for energy?

A

ONLY glucose

Not fats, carbs or protein like other cells

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24
Q

Due to the brain being an OGI, in the post-absorptive state, even tho no new carb is gained, we must…

A

maintain blood glucose concentration sufficient to meet the brain’s requirements

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25
Q

What does failure to maintain blood glucose concentration in the post-absorptive state result in?

A

Hypoglycaemia which can lead to coma and death

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26
Q

How is blood glucose maintained?

A

By synthesising glucose from glycogen (glycogenolysis) or amino acids (gluconeogenesis)

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27
Q

In hyperglycaemia (like in diabetics), what does the body do with the excess glucose?

A

Tries to eject it via urine

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28
Q

How is glucose stored in the body?

A

As glycogen, which is stored in the liver and turns it to fat

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29
Q

What is the NORMAL range of blood glucose?

A

4.2 - 6.3mM

remember 5 mmoles !!

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30
Q

What BG level is considered hypo- and hyper- glycaemia?

A

Under 4 is too low, under 3 is emergency

Around 10/11 is hyper - symptoms develop slowly

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31
Q

Where in the pancreas are hormones released?

A

Islets of Langherhans

32
Q

What are the 4 types of islet cells in the pancreas?

A

Alpha
Beta
Delta
F

33
Q

What hormones do each of the pancreatic islet cells produce?

A 
alpha = GLUCAGON
beta = INSULIN 
delta = SOMATOSTATIN 
F = pancreatic polypeptide (function unknown - may help control nutrient absorption from GIT)
34
Q

What is the fed (absorptive) state dominated by?

A

INSULIN

35
Q

Name 4 processes which increase in the fed state due to insulin

A 
Glucose oxidation
Glycogen synthesis 
Fat synthesis 
Protein synthesis
(BG decreases)
36
Q

What is the fasted (post-absorptive) state dominated by?

A

GLUCAGON

37
Q

Name 3 processes which increase in the fasted (post-absorptive) state when glucagon dominates

A

Glycogenolysis
Gluconeogenesis
Ketogenesis
(BG decreases)

38
Q

What does insulin stimulate?

A

Glucose uptake by cells

39
Q

How is insulin synthesised?

A

As a large preprohormone (preproinsulin), which is then converted to proinsulin in the ER

40
Q

What is the next stage when proinsulin in made?

A

It is then packaged as granules in secretory vesicles; within these vesicles proinsulin is cleaved again to give insulin + C-peptide

41
Q

What then happens to insulin and C-peptide?

A

It is stored in this form until the B cell is activated and secretion occurs

42
Q

What does this step by step process of insulin synthesis and storage tell us about the type of hormone it is?

A

It is a peptide hormone

43
Q

During the absorptive state, what three things enter the blood from the GI tract?

A

Glucose
Amino acids
Fatty acids

44
Q

Both glucose and aa’s stimulate insulin secretion, but what is the major stimulus?

A

Increase in blood glucose concentration

45
Q

Insulin is the ONLY hormone that does what?

A

Lowers BG

46
Q

Where is excess glucose stored?

A 
As glycogen in liver and muscle
As triacyglycerols (TAG) in liver and adipose tissue
47
Q

How are amino acids used?

A

Mainly to make new proteins; also as energy source

48
Q

How are excess amino acids stored?

A

They are converted to fat

49
Q

How are excess fatty acids stored?

A

In the form of triglycerides in adipose tissue and liver

50
Q

Describe in a stepwise manner the control of insulin secretion in situations of high BG

A
  1. High BG level in blood
  2. Glucose enters cells through GLUT and metabolism increases
  3. Increased ATP in cell triggers closure of K-ATP channels
  4. Intracellular K+ rises and depolarises the cell
  5. Voltage dependent Ca2+ channels open and trigger insulin vesicle exocytosis
51
Q

Describe in a stepwise manner the control of insulin secretion in situations of low BG

A
  1. Low BG level in blood
  2. K-ATP channels remain open so K+ ions flow out removing +ve charge from cell
  3. Cell is hyperpolarised
  4. Voltage-gated Ca2+ channels remain closed and insulin is not secreted
52
Q

So what is the main driving force for the release of insulin?

A

Glucose

53
Q

What is the primary action of insulin?

A

Binds to tyrosine kinase receptors on the cell membrane of INSULIN-SENSITIVE tissues to increase glucose uptake by these tissues

54
Q

In muscle + adipose, insulin stimulates mobilisation of…

A

SPECIFIC glucose transporters (GLUT-4) via a signal tranduction cascade

55
Q

Where do GLUT-4 transporters reside?

A

Cytoplasm of cells

56
Q

What does GLUT-4 do when stimulated by insulin?

A

Secretory vesicle migrates to membrane and GLUT-4 is then able to transport glucose into the cell

57
Q

What do GLUT-4 transporters do when insulin stimulation stops?

A

They return to the cytoplasmic pool

58
Q

What is glucose taken up by cells primarily used for?

A

Energy

59
Q

What 2 types of tissue are insulin DEPENDENT? (where other types of tissue do not require it to take up glucose)

A

Muscle

Fat

60
Q

Why are other tissues not insulin dependent?

A

They have other types of GLUT transporters (not GLUT-4)

61
Q

How do beta cells of pancreas and liver take up glucose?

A

GLUT-2 transporters

62
Q

Does insulin directly affect the liver?

A

No

63
Q

Does insulin status affect glucose transport into hepatocytes tho?

A

Yea

64
Q

In the fed state, how does insulin impact glucose transport in hepatocytes?

A

Liver takes up glucose cos insulin activates hexokinase which lowers IC glucose creating a gradient favouring gluocose movement into cells

65
Q

In the fasted state, what does the liver do to increase BG?

A

Synthesises glucose via glucogenolysis and gluconeogenesis

66
Q

Name 6 more actions of insulin (5 are anabolic/inhibit catabolism)

A
  1. Increases glycogen synthesis in muscle + liver
  2. Increases amino acid uptake into muscle
  3. Increases protein synthesis + inhibits proteolysis
  4. Increases triacyglycerolsynthesis in adipocytes + liver
  5. Inhibits the enzymes of gluconeogenesis in the liver
  6. Promtotes K+ ion entry into cells by stimulating Na+/K+ ATPase
67
Q

How are all of the additional roles of insulin possible?

A

Activation of multiple signal transduction pathways associated with the Insulin Receptor

68
Q

What is the half life of insulin?

A

5 mins

69
Q

Once insulin action is complete, what happens to insulin-bound receptors?

A

They are internalised by endocytosis and destroyed by insulin protease (some recycled)

70
Q

Name 5 stimuli which increase insulin release

A
  1. Increased BG
  2. Increased plasma amino acids
  3. Glucagon
  4. Other (incretin) hormones controlling GI secretion + motility
  5. Vagal nerve activity
71
Q

Give examples of other incretin hormones controlling GI secretion + activity

A

Gastrin, secretin, CCK, GLP-1, GIP (released by jejunum and ileum in response to nutrients)

72
Q

Why is glucagon a stimuli for insulin?

A

Insulin is required to take up glucose created via gluconeogenesis stimulated by glucagon

73
Q

What is the purpose of incretin hormones and vagal activity stimulating insulin release?

A

Anticipatory phase - preparation for food

74
Q

Name 4 stimuli which inhibit insulin release

A
  1. Low BG
  2. Somatostatin (GHIH)
  3. Sympathetic alpha 2 effects
  4. Stress (e.g. hypoxia)
75
Q

What does vagal activity stimulate the release of?

A

Major GI hormones

Insulin

76
Q

What does vagal activity stimulating the release of major GI hormones and insulin mean in terms of glucose administration?

A

Insulin response to an IV glucose load is less than the equivalent amount of glucose administered orally

77
Q

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

A

Because oral loading of glucose stimulates insulin release both by direct effect on beta cells AND VAGAL STIMULATION of beta cells (PLUS incretin effects)

*Diabetes & Endocrinology (24 decks)

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