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Endocrine Physiology > The Endocrine Pancreas > Flashcards

The Endocrine Pancreas Flashcards

1
Q

Energy (food) intake is determined by the balance of activity in which two hypothalamic centres?

A

Feeding centre

Satiety centre

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2
Q

What does the feeding centre promote?

A

Feelings of hunger and drive to eat

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3
Q

What does the satiety centre promote?

A

Feelings of fullness by suppressing feeding centre

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4
Q

Two theories about how we control feeding and satiety centres

A

Glucostatic theory

Lipostatic theory

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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

Foot 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 is a hormone released by fat stores/adipose tissue and what does it do?

A

Leptin

Depresses feeding activity

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8
Q

3 categories of energy output

A

Cellular work
Mechanical work
Heat loss

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9
Q

What counts as mechanical work?

A

Movement either on large scale using muscle or intracellularly

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10
Q

What counts as cellular work?

A

Transporting molecules across membranes
growth and repair
storage of energy (e.g. fat, glycogen, ATP synthesis)

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11
Q

What is metabolism?

A

Integration of all biochemical reactions in the body

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12
Q

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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13
Q

What is an anabolic pathway?

A

Build up - net effect of synthesis of large molecules from molecules of smaller size, usually for storage purposes

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14
Q

What is a catabolic pathway?

A

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

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15
Q

Example of a catabolic pathway

A

Glucocorticoid pathway

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16
Q

What state do we enter into after eating and what happens during this?

A

Absorptive state

Ingested nutrients supply the energy needs of the body and the excess is stored.

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17
Q

What type of pathway is the absorptive state?

A

Anabolic

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18
Q

What dominates the anabolic phase?

A

Insulin

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19
Q

When do we enter the post-absorptive state / fasted state?

A

Between meals

Overnight

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20
Q

What happens during the post absorptive / fasted state?

A

The pool of nutrients in the plasma decreases

We rely on body stores to provide energy, releasing this energy

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21
Q

What kind of phase is the post absorptive / fasted state?

A

Catabolic phase

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22
Q

What dominates the post absorptive / fasted phase?

A

Glucagon

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23
Q

What is the brains only energy supply?

A

Glucose

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24
Q

How is the concentration of blood glucose maintained?

A

From glycogen (glucogenolysis) or amino acids (gluconeogenesis)

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25
Q

What effects does hypoglycaemia lead to in the brain?

A

Coma

Death

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26
Q

What is the only organ in the body which has access to blood glucose when the concentration of blood glucose falls below normal range?

A

The brain

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27
Q

What can be stored as fat?

A

Glycerol as fatty acids

Glucose if excess glucose

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28
Q

What is fat broken down into?

A

Free fatty acids

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29
Q

What are carbohydrates broken down into?

A

Glucose

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30
Q

How Is excess glucose stored in normal circumstances?

A

Glycogen in muscle or liver

Triacylglycerols (TAG) in liver and adipose tissue

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31
Q

What is lipogenesis and glycogenesis stimulated by?

A

Insulin

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32
Q

What is gluconeogenesis and glycogenosis stimulated by?

A

Glucagon

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33
Q

What happens if we become short of glucose?

A

Glycogen stores are broken down and new glucose is created from amino acids - glucogenosis and glyconeogenesis

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34
Q

What is required to metabolise glucose?

A

Insulin

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35
Q

Normal range of [BG]

A

4.2 - 6.3mM (80-120mg/dl) / 5 mM

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36
Q

What [BG] is classified as hypoglycaemia?

A

< 3 mM

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37
Q

What two hormones produced in the pancreas are key to the maintenance of a tight range of [BG]?

A

Insulin

Glucagon

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38
Q

How much of the pancreas works as an exocrine gland and how much as an endocrine gland?

A

99% as exocrine - releasing enzymes and NaHCO3 via ducts into alimentary canal to support digestion
1% has endocrine function

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39
Q

Where are the hormones produced in the pancreas?

A

Islets of Langerhans

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40
Q

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

A

A cells
B cells
Gamma cells
F cels

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41
Q

What do A islet cells produce?

A

Glucagon

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42
Q

What do B islet cells produce?

A

Insulin

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43
Q

What do gamma islet cells produce?

A

Somatostatin

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44
Q

What do F islet cells produce?

A

Pancreatic polypeptide

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45
Q

What type of hormone is insulin?

A

Peptide hormone

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46
Q

Function of insulin

A

Stimulates glucose uptake by cells

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47
Q

What is insulin originally synthesised as and what is this converted into?

A

A large preprohormone - preproinsulin which is then converted to proinsulin in the ER

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48
Q

How is proinsulin stored?

A

Packaged as granules in secretory vesicles.

When cleaved stored as insulin and C peptide until activation and secretion occurs

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49
Q

What is proinsulin cleaved into?

A

Insulin and C peptide

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50
Q

What is the only hormone which lowers the [BG]?

A

Insulin

51
Q

What do most cells use as their energy source during the absorptive state?

A

Glucose

52
Q

What are excess amino acids converted into?

A

Fat

53
Q

How are fatty acids stored?

A

In the form of triglycerides in adipose tissue and liver

54
Q

What type of hormone is glucagon?

A

Peptide hormone

55
Q

What is the main function of glucagon?

A

To raise blood glucose

56
Q

What does glucagon mainly act on?

A

The liver

57
Q

Control of blood glucose depends on the balance between what two hormones?

A

Insulin

Glucagon

58
Q

What processes happen in blood when insulin dominates in the fed state?

A

Increased glucose oxidation
Increased glycogen synthesis
Increased fat synthesis
Increased protein synthesis

59
Q

What processes happen in the blood in the fasted state where glucagon dominates?

A

Increased glycogenolysis
Increased gluconeogenesis
Increased ketogensis

60
Q

When glucagon dominates, what happens to glucose levels in the blood?

A

increased glucose levels in plasma as it is released into plasma

61
Q

How is insulin released into the plasma from the islet cells?

A

When glucose is abundant it enters cells through glucose transport proteins (GLUT) and metabolism increases
This increases [ATP] within the cell causing the KATP channel to close.
Intracellular [K+] rises, depolarising the cell
Voltage dependent Ca2+ channels open and trigger insulin vesicle exocytosis into the circulation

62
Q

What occurs in the blood and the cells for insulin not to be secreted?

A

When [BG] is low, [ATP] is low and so KATP channels are open so K+ ions flow out removing the +ve charge from the cell and hyperpolarising it
So the voltage gated Ca2+ channels remain closed
so insulin is not secreted

63
Q

What does insulin bind to on the cells?

A

Tyrosine kinase receptors on the cell membrane of insulin sensitive tissues

64
Q

What are the two insulin sensitive tissues?

A

Muscle

Adipose tissue

65
Q

What does insulin stimulate to happen to the cells?

A

Stimulates mobilisation of specific glucose transporters (GLUT-4)

66
Q

Where does GLUT 4 reside usually?

A

In the cytoplasm of unstimulated muscle and adipose cells

67
Q

What does GLUT 4 do once stimulated by insulin?

A

Migrates to the membrane and then transports glucose into the cell

68
Q

What happens to GLUT 4 transporters when the insulin stimulation stops?

A

They return to the cytoplasmic pool

69
Q

What is the glucose taken up by cells primarily used for?

A

Energy

70
Q

How much of total body weight does muscle make up?

A

40%

71
Q

How much of total body weight does fat make up?

A

20-25%

72
Q

What are other NON-insulin dependent GLUT-transporters and where are they found?

A 
GLUT-1 = many tissues e.g. brain, kidney, RBCs
GLUT-3 = similar
GLUT-2 = B cells of pancreas and liver
73
Q

How does glucose enter the liver?

A

Down a concentration gradient through GLUT-2 transporters (NON-insulin dependent)

74
Q

Insulin relationship to liver

A

Insulin has no direct effect on liver

Although glucose transport into hepatocytes is affected by insulin status

75
Q

Actions of insulin

A

Move glucose into cells
Increases glycogen synthesis in muscle and liver (stimulates glycogen synthase and inhibits glycogen phosphorylase)
Increases amino acid uptake into muscle, promoting protein synthesis (anabolic)
Increases protein synthesis and inhibits proteolysis
Increases triacylglycerol synthesis in adipocytes and liver i.e. stimulates lipogenesis and inhibits lipolysis
Inhibits the enzymes of gluconeogenesis in the liver
Has permissive effect on growth hormone
Promotes K+ ion entry into cells by stimulating Na/K ATPase.

76
Q

Approx. half life of insulin and what is it principally degraded by?

A

5 mins

Liver and kidneys

77
Q

What happens to insulin bound receptors once insulin action is complete?

A

They are internalised by endocytosis and destroyed by insulin protease, some recycled

78
Q

What stimuli cause increased insulin release?

A 
Increased [BG]
Increased [amino acids] in plasma
Glucagon 
Other (incretin) hormones controlling GI secretion and motility e.g. gastrin, secretin, CCK - insulin prevents glucose surge when absorption occurs
Vagal nerve activity
79
Q

Stimuli which inhibit insulin release

A

Low [BG]
Somatostatin (GHIH)
Sympathetic a2 effects
Stress e.g. hypoxia

80
Q

What does oral loading of same amount of glucose compared to IV lead to? Why?

A

Leads to increased insulin by both direct effect on B cells and vagal stimulation of B cells, plus incretin effects
Because vagal activity stimulates release of major GI hormones as well as insulin release

81
Q

What hormones are part of the glucose counter-regulatory control system?

A

Glucagon
Epinephrine
Cortisol
GH

82
Q

What are glucagon receptors?

A

G-protein coupled receptors linked to adenylate cyclase/cAMP system

83
Q

Effects of glucagon

A

Increased glycogenolysis
Increased gluconeogenesis (substrates amino acids and glycerol)
Formation of ketones from fatty acids (lipolysis)

84
Q

Where do all the processes as a result of glucagon occur?

A

The liver

85
Q

Secretion of glucagon

A

Relatively constant

Increases dramatically when [BG] <5.6mM so doesn’t wait until levels are dangerously low

86
Q

What are amino acids a potent stimulus for?

A

Glucagon secretion

87
Q

What do amino acids in the plasma release?

A

Both insulin and glucagon

88
Q

What is the brain also known as in endocrine?

A

Obligatory glucose user

89
Q

What can most other tissues readily use to produce energy?

A

FFAs

Ketones

90
Q

Stimuli that promote glucagon release

A 
Low [BG]
High [amino acids]
Sympathetic innervation and epinephrine, B2 effects 
Cortisol 
Stress e.g. exercise, infection
91
Q

Stimuli that inhibit glucagon release

A

Glucose
Free fatty acids (FFAs) and ketones
Insulin (fails in diabetes so glucagon levels rise despite high [BG])
Somatostatin

92
Q

Effect of an increase in parasympathetic activity (vagus) of islet cells

A

Increase in insulin and to a lesser extent decrease in glucagon, in association with the anticipatory phase of digestion

93
Q

Effect of an increase in sympathetic activation of islet cells

A

promotes glucose mobilisation -> increase in glucagon, increase in epinephrine and inhibition of insulin, all appropriate for a fight or flight response

94
Q

What type of hormone is somatostatin?

A

Peptide hormone

95
Q

Where is somatostatin (GHIH) secreted from?

A

D cells of pancreas

Hypothalamus

96
Q

What is the main action of the pancreatic somatostatin?

A

Inhibit activity in the GI tract

97
Q

What does somatostatin suppress the release of in a paracrine fashion?

A

Both insulin and glucagon

98
Q

What does GHIH inhibit the secretion of from the anterior pituitary?

A

Growth hormone

99
Q

What happens to the entry of glucose into muscle during exercise?

A

It is increased during exercise, even in the absence of insulin

100
Q

Effect of exercise on insulin

A

Increases insulin sensitivity of muscle and causes an insulin-independent increases in the number of GLUT-4 transporters incorporated into the muscle membrane

101
Q

Effects of prolonged exercise on insulin sensitivity

A

Increases it

102
Q

What are excess fatty acids converted into and by what?

A

Ketone bodies

By the liver

103
Q

What do ketone bodies provide as an additional energy source?

A

Muscle

Brain

104
Q

After a period of starvation, what does the brain adapt to use?

A

Ketones

105
Q

How are ketones produced?

A

Through beta oxidation in the liver from free fatty acids

106
Q

DM involves the loss of control of what?

A

Blood glucose levels

107
Q

Two types of DM

A

Type I

Type II

108
Q

Pathology of Type I DM

A

Autoimmune destruction of the pancreatic B-cells

Destroys the ability to produce insulin and seriously compromises the patients ability to absorb glucose from the plasma

109
Q

What % of diabetic patients are insulin dependent?

A

10%

110
Q

What is T1DM also known as?

A

Insulin dependent diabetes mellitus (IDDM)

111
Q

What is T2DM also known as?

A

Non insulin dependent diabetes mellitus (NIDDM)

112
Q

Pathology of type II diabetes

A

Peripheral tissues become insensitive to insulin = insulin resistance
Muscle and fat no longer respond to normal levels of insulin
Either due to an abnormal response to insulin receptors in these tissues or a reduction in their number
B cells remain intact and appear normal, there may even be hyperinsulinaemia

113
Q

What % of diabetic patients are insulin resistant? (NIDDM)

A

90%

114
Q

What is T2DM typically associated with?

A

Obesity

115
Q

What age does T2DM usually appear?

A

> 40 y/o but age decreasing

116
Q

What are major contributors to T2DM?

A

High sugar and animal fat diet

Little exercise

117
Q

Treatment of T2DM

A

Initial - exercise and dietary changes
If fails - oral hypoglycaemic drugs (metformin)
Sulphonylureas
Eventually may end up taking insulin

118
Q

What is the diagnostic criterion for diabetes?

A

Hyperglycaemia (elevated [BG])

119
Q

Describe the glucose tolerance test

A

Patient ingests glucose load after fasting [BG] measured

[BG] will normally return to fasting levels within an hour, elevation after 2 hours is indicative of diabetes

120
Q

Does the glucose tolerance test distinguish between T1DM and T2DM?

A

No

121
Q

Pathology of ketoacidosis in T1DM

A

FFAs can be converted to ketones for additional energy source for muscle and brain when energy sources are scarce
In poorly controlled IDDM a lack of insulin depresses ketone body uptake.
They build up rapidly in plasma and because they are acidic create life threatening acidosis (ketoacidosis) with plasma pH < 7.1

122
Q

How are ketones detectable?

A

Urine

Produce distinctive acetone smell to breath

123
Q

What are hyperglycaemic long term diabetic complications?

A

Retinopathy
Neuropathy
Nephropathy
Cardiovascular disease

Endocrine Physiology (8 decks)

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