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The endocrine pancreas Flashcards

1
Q

what is body energy equal to?

A

energy intake – energy output

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2
Q

what is energy (food) intake determines by?

A

balance of activity in two hypothalamic centres:

Feeding Centre - promotes feelings of hunger and drive to eat

Satiety Centre – promotes feelings of fullness by suppressing the Feeding Centre (insulin sensitive)

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3
Q

what is the feeding centre?

A

promotes feelings of hunger and drive to eat

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4
Q

what is the satiety centre?

A

promotes feelings of fullness by suppressing the Feeding Centre (insulin sensitive)

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5
Q

what is the activity of feeding and satiety centre controlled by?

A

Activity in each is controlled by a complex balance of neural and chemical signals as well as the presence of nutrients in plasma.

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6
Q

what is 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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7
Q

what is lipostatic theory?

A

food intake is determined by fat stores: as fat stores increase, the drive to eat decreases (- feeding centre; + Satiety Centre). Leptin is a peptide hormone released by fat stores which depresses feeding activity.

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8
Q

ehat does energy output describe?

A

all the processes we perform simply in order to stay alive, and those that we perform voluntarily, as well as the heat loss associated with these.

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9
Q

what are three categories of energy output?

A

Cellular work – transporting molecules across membranes; growth and repair; storage of energy (eg. fat, glycogen, ATP synthesis).

Mechanical work – movement, either on large scale using muscle or intracellularly.

Heat loss – associated with cellular and mechanical work accounts for half our energy output.

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10
Q

what is metabolism?

A

integration of all biochemical reactions in the body

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11
Q

what are the three elements of metabolism?

A

Extracting energy from nutrients in food
Storing that energy
Utilising that energy for work

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12
Q

what is an anabolic pathway?

A

Build Up. Net effect is synthesis of large molecules from smaller ones, usually for storage purposes.

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13
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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14
Q

what state is entered following eating?

A

Absorptive State

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15
Q

what is the absorptive state?

A

where ingested nutrients supply the energy needs of the body and excess is stored. This is an anabolic phase.

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16
Q

what do we enter between meals and overnight causing the pool of nutrients in the plasma to decrease?

A

post-absorptive State (aka Fasted State) where we rely on body stores to provide energy. This is a catabolic phase.

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17
Q

what is the brain described as?

A

obligatory glucose utiliser

Most cells can use fats, carbohydrates or protein for energy but the brain can only use glucose (except in extreme starvation

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18
Q

what must happen in the post absorpative state due to the brain being a obligatory glucose utiliser?

A

so in the post-absorptive state, even though no new carbohydrate is gained by the body we MUST maintain blood glucose concentration [BG] sufficient to meet the brain’s requirements.

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19
Q

what would failure to do this mean?

A

hypoglycaemia (low blood glucose) which can lead to coma and death.

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20
Q

how is blood glucose maintained?

A

by synthesising glucose from glycogen (glycogenolysis) or amino acids (gluconeogensis) (new glucose from amino acids).

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21
Q

what is the normal range of blood glucose?

A

Normal range of [BG] = 4.2-6.3mM (80-120mg/dl)

5 mmoles useful to remember

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22
Q

what is blood glucose for a hypoglycemic?

A

[BG] < 3mM

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23
Q

what two endocrine hormones produced by the pancreas maintains blood pressure?

A

Insulin and Glucagon

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24
Q

what are endocrine hormones released from the pancreas?

A

99% of the pancreas operates as an exocrine gland releasing enzymes and NaHCO3 via ducts into the alimentary canal to support digestion.

Only 1% of the pancreas has endocrine function. It’s hormones are produced in the Islets of Langerhans.

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25
Q

what are the four types of islets of langerhans cells?

A

α, β, δ & F.

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26
Q

what do α cells produce?

A

glucagon

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27
Q

what do β cells produce?

A

insulin

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28
Q

what do δ cells produce?

A

somatostatin

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29
Q

what do F cells produce?

A

pancreatic polypeptide (function not really known, may help control of nutrient absorption from GIT.)

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30
Q

if insulin is in excess to glucagon what happens?

A

glucose taken up by cells from plasma blood glucose decreases

increase in:
glucose oxidation
glcogen synthesis
fat synthesis
protein synthesis

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31
Q

if glucagon is in excess to insulin what happens?

A

Glucose released into plasma from stores ([BG] increases)

increase in:
glycogenolysis
gluconeogensis
ketogenesis

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32
Q

what type of hormone is insulin?

A

Peptide hormone

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33
Q

what is insulin produced by?

A

produced by pancreatic β cells.

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34
Q

what is the function of insulin?

A

Stimulates glucose uptake by cells.

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35
Q

describe the mechanism of action of insulin?

A

Synthesized as a large preprohormone, preproinsulin, which is then converted to proinsulin in the ER.
Proinsulin is then packaged as granules in secretory vesicles. Within the granules the proinsulin is cleaved again to give insulin and C-peptide. Insulin is stored in this form until the β cell is activated and secretion occurs.

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36
Q

what happens during the absorpative phase?

A

glucose, amino acids (aa) and fatty acids enter blood from GI Tract.

Both glucose and aa’s stimulate insulin secretion but the major stimulus is blood glucose concentration.

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37
Q

what is the only hormone that lowers blood glucose?

A

insulin

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38
Q

what are the different potential fates of glucose?

A

Most cells use glucose as their energy source during the absorptive state. Any excess is stored as glycogen in liver and muscle, and as triacylglycerols (TAG) in liver and adipose tissue.

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39
Q

what are amino acids mainky used for?

A

to make new proteins with excess being converted to fat.

Also form an energy source.

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40
Q

how are fatty acids stored?

A

stored in the form of triglycerides in adipose tissue and liver.

41
Q

describe the mechanism of control of insulin secretion by blood glucose?

A

β-cells have a specific type of K+ ion channel that is sensitive to the [ATP] within the cell = KATP channel.

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.

42
Q

what happens to Katp channels when blood glucose is low?

A

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

43
Q

what is the primary action of insulin?

A

Binds to tyrosine kinase receptors on the cell membrane of insulin-dependent tissues to increase glucose uptake by these tissues.

44
Q

what is the only hormone that lowers blood glucose?

A

insulin

45
Q

what does insulin do in muscle and adipose tissue?

A

insulin stimulates the mobilization of specific glucose transporters, GLUT-4, which reside in the cytoplasm of these cells.

When stimulated by insulin GLUT4 migrates to the membrane and is then able to transport glucose into the cell. When insulin stimulation stops, the GLUT-4 transporters return to the cytoplasmic pool.

The glucose taken up by cells is primarily used for energy.

46
Q

do most types of tissue require insulin to take up glucose?

A

Most types of tissue do NOT require insulin to take up glucose, ONLY muscle and fat are insulin dependent.

47
Q

what percentage of the body is made up of muscle and fat?

A

Muscle is ≈ 40% BW and fat ≈ 20-25% (in normality).

48
Q

In other tissues glucose uptake is via other GLUT-transporters, which are NOT insulin-dependent.

What are these transporters?

A

GLUT-1 Basal glucose uptake in many tissues eg brain, kidney and red blood cells. GLUT-3 Similar GLUT-2 β-cells of pancreas and liver

49
Q

is the liver an insulin dependent tissue?

A

no

50
Q

how does the liver take up glucose?

A

Liver takes up glucose by GLUT 2 transporters, which are insulin independent.

Glucose enters down concentration gradient.

51
Q

although insulin has no direct effect on the liver what is glucose transport into hepatocytes affected by?

A

insulin status

52
Q

what is the mechanism of glucose transport in hepatocytes in a fed state?

A

liver takes up glucose because insulin activates hexokinase which lowers [glucose]ic creating a gradient favouring glucose movement into the cells.

53
Q

what is the mechanism of glucose transport in hepatocytes in a fasted state?

A

liver synthesises glucose via glycogenolysis and gluconeogenesis, increasing [glucose]ic creating a gradient favouring glucose movement out of the cells into the blood.

54
Q

what are the 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 i.e. stimulates lipogenesis and inhibits lipolysis.

Inhibits the enzymes of gluconeogenesis in the liver

55
Q

actions of insulin:

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 i.e. stimulates lipogenesis and inhibits lipolysis.

Inhibits the enzymes of gluconeogenesis in the liver

are all what type of process?

A

anabolic processes – laying down energy stores – or inhibit catabolism

56
Q

what effect does insulin have on growth hormone and K entry into cells?

A

Has a permissive effect on Growth Hormone (see GH lecture)

Promotes K+ ion entry into cells by stimulating Na+/K+ ATPase.

57
Q

what is the half life of insulin?

A

5 minutes and is degraded principally in the liver and kidneys.

58
Q

what happens to complete insulin bound receptors after insulin action is complete?

A

Once insulin action is complete insulin-bound receptors are internalised by endocytosis and destroyed by insulin protease, some recycled.

59
Q

what change in blood pressure would stimulate insulin release?

A

Increased [BG]

60
Q

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 eg gastrin, secretin, CCK, GLP-1, GIP

vagal nerve activity

have what effect on insulin release?

A

increases insulin release

61
Q

what stimuli inhibit insulin release?

A

Low [BG]

Somatostatin (GHIH)

Sympathetic α2 effects

Stress e.g. hypoxia

62
Q

what does vagal activity stimulate the release of?

A

major GI hormones, and also directly stimulates insulin release, therefore meaning that the insulin response to an intravenous glucose load is less than the equivalent amount of glucose administered orally

63
Q

why is the insulin response from an intravenous glucose load is less than the equivalent amount of glucose administered orally?

A

Vagal activity stimulates release of major GI hormones

64
Q

describe IV loading of glucose versus oral loading?

A

i.v. glucose → ↑ insulin by direct effect of ↑ glucose on β cells.

Oral loading of same amount of glucose → ↑ insulin by both direct effect on β cells and vagal stimulation of β cells, plus incretin effects!

65
Q

what does control of glucose depend upon the balance inbetween?

A

Depends on balance between insulin and glucagon

66
Q

what is glucagon?

A

Peptide hormone produced by α-cells of the pancreatic islet cells in same fashion as all peptide hormones.

67
Q

what is the primary purpose of glucagon?

A

to raise blood glucose. It is a glucose-mobilizing hormone, acting mainly on the liver.

68
Q

what are the actions of glucagon?

A

Primarily opposes the action of insulin, forming part of the glucose counter-regulatory control system which includes the hormones epinephrine, cortisol and GH.

69
Q

when is glucagon most active?

A

It is most active in the post-absorptive state.

70
Q

what are glucagon receptors?

A

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

71
Q

when activated what effect do glucagon receptors result in?

A

when activated phosphorylate specific liver enzymes resulting in:

increased glycogenolysis

increased gluconeogenesis
(substrates: aa’s and glycerol (lipolysis))

formation of ketones from fatty acids (lipolysis)

All these processes occur in the liver.
** Net result is elevated [BG]**

72
Q

describe the response to decreased plasma glucose?

A
73
Q

Amino acids are also a potent stimulus for glucagon secretion. What would happen if they weren’t?

A

Amino acids stimulate insulin release which in the absence of glucagon would stimulate glucose uptake into cells, dramatically lowering [BG].
Potentially catastrophic for the brain.

74
Q

changes in [BG] have opposite effects on insulin and glucagon, what are they?

A

↑glucose → ↑ insulin and ↓ glucagon ↓ glucose → ↑ glucagon and ↓ insulin

75
Q

Amino acids in the plasma stimulate release of…

A

both insulin and glucagon.

This is an adaptation to adjust for the composition of a meal very high in protein (typical of carnivores).

76
Q

what effect do amino acids have on a high protein meal with very little carbohydrate?

A

aas → ↑ insulin → ↓ [BG] aas → ↑ glucagon → ↑ [BG]

If it were not for the effect of aas on glucagon then the insulin-stimulating effects of aas would result in very low [BG]. This is counteracted by the glucose mobilizing effects of glucagon and so [BG] is maintained.

77
Q

what stimuli promote glucagon release?

A

Low [BG] (<5mM)

High [amino acids] . Prevents hypoglycaemia following insulin release in response to aa.

sympathetic innervation and epinephrine, β2 effect
cortisol

stress e.g. exercise, infection

78
Q

what stimuli inhibit glucagon release?

A

glucose
free fatty acids (FFA) and ketones
insulin (fails in diabetes so glucagon levels rise despite high [BG] )
somatostatin

79
Q

what is the parasympathetic innervation of islet cells?

A

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

80
Q

what is the sympathetic innervation of islet cells?

A

↑ glucagon, ↑ epinephrine and inhibition of insulin, all appropriate for fight or flight response.

81
Q

what effect does glucagon have on

A

increases liver glycogenolysis
increases gluconeogenesis
increases lipolysis

82
Q

what effect does epinephrine have on

A

increases muscle glycogenolysis
increases liver glycogenolysis
increases gluconeogenesis
increases lipolysis

83
Q

what effect does cortisol have on

A

increases gluconeogenesis
increased inhibition of glucose uptake
increases lipolysis
increases protein catabolism

84
Q

what effect does growth hormone have on

A

increases gluconeogensis
increase in inhibition of glucose uptake
increase in lipolysis

85
Q

what is somatostatin?

A

Peptide hormone, secreted by D-cells of the pancreas (and hypothalamus aka GHIH).

86
Q

what is the main pancreatic function of somatostatin?

A

inhibit activity in the GI Tract. Function appears to be to slow down absorption of nutrients to prevent exaggerated peaks in plasma concentrations.

87
Q

how can synthetic somatostatin be used clinically?

A

to help patients with life-threatening diarrhoea associated with gut or pancreatic tumours).

88
Q

how does somatostatin effect insulin and glucagon?

A

SS strongly suppresses the release of both insulin and glucagon in a paracrine fashion

89
Q

how does pancreatic ss secreting tumours affect the patient?

A

Patients with pancreatic SS-secreting tumours develop the symptoms of diabetes which disappear when the tumour is removed.

90
Q

describe effect of glucagon, insulin and SS on one another?

A
91
Q

what effect does excersize have on blood glucose

A

The entry of glucose into skeletal muscle is increased during exercise, even in the absence of insulin. There is an insulin-independent increase in the number of GLUT-4 transporters incorporated into the muscle membrane.

92
Q

does excersize increase the insulin sensitivity of muscle?

A

yes

93
Q

how long does the effect of excersize persist?

A

several hours after exercise and regular exercise can produce prolonged increases in insulin sensitivity.

94
Q

how is glucose transported in non active muscle?

A

insulin binds to its receptor, which then leads to glucose transporters, GLUT4, migrating to the cell membrane, allowing glucose to enter.

95
Q

how is glucose transported in active muscle?

A

In active muscle, GLUT4 transporters can migrate to the membrane without insulin being present, so exercise causes glucose uptake independently of insulin.

It also increases the sensitivity of the muscle to insulin.

96
Q

how does the body function in a state of starvation?

A

When nutrients are scarce, body relies on stores for energy – when adipose tissue is broken down fatty acids are released.

FFA’s can be readily used by most tissues to produce energy and liver will convert excess to ketone bodies which provides an additional source for muscle and brain!

97
Q

is ketone body uptake insulin dependent?

A

yes

98
Q
A

Endocrine (35 decks)

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