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ZA - Endocrine System > The Endocrine Pancreas > Flashcards

The Endocrine Pancreas Flashcards

1
Q

Body energy = X - Y

A

Energy intake - energy output

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2
Q

What two hypothalmic centres control energy intake?

A

Feeding centre - Promotes feeling of hunger and drive to eat

Satiety centre - Promotes feelings of fullness by suppressing feeding centres

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3
Q

What is the glucostatic theory ?

A

As Blood Glucose increases the drive to eat decreases

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4
Q

What is the lipostatic theory ?

A

As fat stores increase the drive to eat decreases

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5
Q

What is leptin?

A

A peptide hormone which is released from fat cells and suppresses feeding activity

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6
Q

What are the 3 categories of energy output?

A

Cellular work
Mechanical work
Heat loss

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7
Q

What does cellular work involve?

A

Transporting molecules across membranes
Growth and repair
Storage of energy via fat, glycogen, ATP

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8
Q

What is mechanical work?

A

Movement via muscle or intracellular movement

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9
Q

What accounts for half of energy output?

A

Heat loss

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10
Q

What to anabolic pathways do?

A

Build up smaller molecules into larger ones for storage

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11
Q

What do catabolic pathways do?

A

Break down large molecules into smaller ones to release energy

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12
Q

What happens after we eat?

A

We enter into an absorptive state which is anabolic

If energy input exceeds bodies need excess is stored

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13
Q

What happens between meals and overnight?

A

A post absorptive/fasting state

Bodies stores give energy - catabolic state

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14
Q

What does 99% of the pancreas operate as?

A

An exocrine gland that releases enzymes and Sodium Bicarbonate into the GI tract to support digestion

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15
Q

What does the 1% do?

A

Functions as endocrine

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16
Q

Where is the pancreas’ hormones made?

A

In islets of langerhans - tiny clusters of cells

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17
Q

4 types of islet cells and their products?

A

Alpha - glucagon
Beta - insulin
Delta - Somatostatin
F - pancreatic polypeptide

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18
Q

What is the function of pancreatic polypeptide?

A

Not really known

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19
Q

What organ is a obligatory glucose utiliser and what does this mean?

A

The brain

Means it can only use glucose for energy

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20
Q

The brain can use fats, carbs and proteins for energy when glucose is low - T or F

A

False - can only use ketones

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21
Q

How does the brain get glucose in the fasting state?

A

BG conc. is maintained by making glucose from glycogenolysis or gluconeogenesis

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22
Q

What is glycogenolysis and gluconeogenesis

A

GGL - glycogen to glucose

GNG - amino acids and non-carbs

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23
Q

What is normal BG conc?

A

4.2-6.3 mM
or
80-120 mg/dl

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24
Q

When is a patient hypoglycemic?

A

BG is lower than 3mM

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25
Q

What type of hormone is insulin?

A

A peptide hormone

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26
Q

How is insulin made?

A

Synthesised as a large preporhormone - then cleaved into proinsulin by ER

Proinsulin stored as granules in secretory vesicles

Inside the granule proinsulin is cleaved to form insulin and the fragment c-peptide

It is stored in this form til the B-cell is activated and it will be secreted

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27
Q

What does insulin do?

A

Stimulates glucose uptake by cells decreasing BG conc.

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28
Q

Do any other hormones decrease blood glucose?

A

No only insulin

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29
Q

What stimulates insulin secretion?

A

Glucose (BG most important) and amino acids

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30
Q

What happens to excess glucose?

A

Stored as glycogen in liver and muscle and as triacylglyceride in liver and adipose tissue

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31
Q

What are amino acids converted to in excess?

A

Fat

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32
Q

What are fatty acids stored as and where?

A

TAG in adipose tissue and liver

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33
Q

What causes insulin to be secreted from cells when BG conc. is high?

A

When glucose is abundant in blood it enters cells via GLUT transporters and metabolism increases

This increases ATP in the cell

This closes the K-ATP channel causing K+ to rise in the cell depolarising it

This leads to voltage dependant Ca2+ channels to open triggering insulin vesicle exocytosis into cirulation

34
Q

What happens to stop insulin secretion when BG conc. is low?

A

Low BG conc = low ATP in cell

Causes K-ATP channels to open letting K+ leave the cell causing hyperpolarisation

This closes the Ca2+ channels and stops insulin secretion

35
Q

What is the primary action of insulin?

A

Binds to tyrosine kinase receptors of the cell membrane of insulin-sensitive tissues

This stimulates GLUT-4 which resides in muscle and adipose tissue cytoplasms

This leads to increases in glucose uptake for muscles and adipose tissue

36
Q

What tissues are insulin sensitive and what transporter do they use?

A

Muscle and fat

GLUT-4

37
Q

What does GLUT-1 and GLUT-3 do?

A

Non insulin-dependent glucose uptake in many tissues such as brain, kidney, RBCs

38
Q

What does GLUT-2 do?

A

Glucose uptake in B-cells of pancreas and liver

39
Q

Does insulin have any direct effect on the livers glucose uptake?

A

No - is independent of insulin using GLUT-2 and a gradient

40
Q

How does insulin indirectly effect the livers glucose uptake?

A

Glucose transported into hepatocytes is still affected by insulin status

In the fed state insulin binds to liver cells which causes intracellular glucose to convert into glucose-6-phosphate to maintain the gradient

41
Q

What happens to liver cells in the fasted state?

A

In the fasted state - liver makes glucose via glycogenolysis and gluconeogenesis creating a glucose gradient that moves glucose out into the blood

42
Q

What are some additional actions of insulin?

A

Increases glycogen synthesis
Increases amino acid uptake/protein synthesis
Increases TAG and lipocyte synthesis
Has permissive effect on GH

Inhibits gluconeogensis in liver
Promotes K+ ion entry into cells by stimulating the K/Na-ATPase

43
Q

What increases insulin release?

A 
Increase in BG conc.
Increase in AA conc.
Glucagon (in ketosis)
Other incretin hormones 
Vagal activity
44
Q

Why does glucagon stimulate insulin when it has the opposite affects?

A

Insulin needed for uptake of glucose made from gluconeogenesis

45
Q

What are incretin hormones?

A

Hormones that stimulate a decrease in BG conc.

46
Q

Where are incretin hormones released? In response to what and why?

A

Jejunem and ileum in response to nutrients

Released so that an early insulin response prevents a BG surge once the nutrients are absorbed

47
Q

Name some incretin hormones?

A 
Secretin 
CCK
GLP-1
GIP
Gastrin
48
Q

Does vagal activity release insulin when glucose is taken orally or via IV?

A

Orally so insulin response via IV will be less than orally

49
Q

Why does oral glucose increase insulin response more than IV glucose?

A

In IV only b-cells release insulin

In oral - insulin increased via b-cells, vagal activity and incretin horomes

50
Q

What stimuli inhibit insulin release?

A

Low BG conc
Somatostatin
Sympathetic alpha 2 effects
Stress - hypoxia

51
Q

What type of hormone is glucagon? Where is it made and what does it do?

A

Peptide
Alpha cells
Raise BG conc.

52
Q

Where does glucagon mainly act?

A

Liver

53
Q

What is glucagon’s plasma half-life? What is it degraded by?

A

5-10 mins

By liver

54
Q

What is the glucose counter-regulatory control system and what hormones does it involve? When is the system most active?

A

System that opposes action of insulin

Glycogen
Adrenaline
Cortisol
GH

Fasting state

55
Q

What type of receptors are glucagon receptors? What happens once they activate?

A

GPCRs linked to the adenylate-cyclase/cAMP system

Receptor phosphorylates specific liver enzymes

56
Q

What does the phosphorylation of these liver enzymes cause?

A

Increases glycogenolysis and gluconeogenesis

Forms ketones from fatty acids (lipolysis)

This causes increased BG conc.

57
Q

Is glucagon secretion constant? When does it spike?

A

Yes it is quite constant but spikes when BG conc. is less than 5.6 mM

58
Q

What is a more significant measurement of glucagon than just looking at its blood conc?

A

It’s ratio to insulin

59
Q

How do AAs effect glucagon secretion?

A

Stimulates it

60
Q

Why do AAs stimulate glucagon and insulin?

A

To adjust for a meal very high in proteins with no carbs to stop insulin lowering BG levels to dangerous levels without the carbs to replace it

61
Q

List things that promote glucagon release.

A 
Low BG
AAs
Sympathetic innervation and adrenaline on B2 receptors
Cortisol
Stress - exercise or infection
62
Q

List things that inhibit glucagon release.

A

High blood glucose
Free fatty acids and ketones
Insulin
Somatostatin

63
Q

What inbitory mechanism for glucagon fails in diabetes resulting in very high BG conc?

A

Insulin no longer inhibits glucagon secretion so it will secrete rising BG

64
Q

Describe the ANS innervation of islet cells.

A

Parasympathetic activity via vagus nerve leads to:

Increased insulin and small increase in glucagon in anticipation of digestion

Sympathetic innervation - increase in glucagon and adrenaline, inhibition of insulin

65
Q

In summary glucagon causes…

A

Liver glycogenolysis

Gluconeogenesis

66
Q

Adrenaline causes…

A

Muscle and Liver glycogenolysis
Gluconeogenesis
Lipolysis

67
Q

Cortisol causes…

A

Gluconeogenesis
Inhibition of glucose uptake
Lipolysis
Protein catabolism

68
Q

GH causes…

A

Gluconeogenesis
Inhibition of glucose uptake
Lipolysis

69
Q

What type of hormone is somatostatin?

A

A peptide hormone

70
Q

What cells secrete somatostatin?

A

D cells of the pancreas

Hypothalmic cells

71
Q

What is another name for somatostatin?

A

GH inhibiting hormone - inhibits GH release from AP gland

72
Q

Pancreatic function of somatostatin?

A

Inhibit activity in the GI tract

Slows down absorption of nutrients to prevent exaggerated peaks in plasma conc.

73
Q

What can synthetic somatostatin be used for?

A

Help patients with life threatening diarrhoea associated with gut or pancreatic tumours

74
Q

Is somatostatin a counter-regulatory hormone in controlling glucose?

A

No but it does strongly supress release on insulin and glucagon in a paracrine chemical fashion (locally)

75
Q

What do patients with pancreatic somatostatin secreting tumours present with?

A

Symptoms of diabetes that go away after tumour is removed

76
Q

How does exercise disrupt the steady state? How long do these effects last?

A

During exercise glucose entry into skeletal muscle is increased even in absence of insulin

Exercise also increases insulin sensitivity of muscle

Effects last for several hours

77
Q

How does exercise increase muscle sensitivity to insulin?

A

GLUT-4 transporters can migrate to the membrane without insulin being present causing increased sensitivity to insulin

78
Q

How does starvation disrupt the steady state ?

A

Adipose tissue –> FFAs –> Ketones

FFAs can be used readily by most tissues

79
Q

What does the starvation response spare?

A

Muscle tissue from being broken down by gluconeogenesis

80
Q

Why is muscle breakdown bad?

A

Leaves body prone to infections and weak

ZA - Endocrine System (21 decks)

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