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MD4001 Physiology > Pancreas: Exocrine and Endocrine Functions > Flashcards

Pancreas: Exocrine and Endocrine Functions Flashcards

1
Q

What part of the pancreas has an exocrine function?

A

Pancreatic acini

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2
Q

What part of the pancreas has an endocrine function?

A

Islets of langerhans

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3
Q

How much of the total mass of the pancreas is made up from islets of langerhans?

A

~ < 2%

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4
Q

What are the different cell types inside the islets of Langerhans?

A
  • A / alpha / alpha 2 cells (glucagon)
  • B / Beta cells (insulin)
  • D / alpha 1 / gamma / delta cells (somatostatin)
  • F (pancreatic polypeptide)
  • Epsilon cells (grelin)
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5
Q

What is the structure of glucagon?

A

29 amino acid linear polypeptide

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6
Q

What is the structure of insulin?

A

21 amino acid (A chain) and 30 amino acids (B chain) peptides linked by 2 disulphode bonds

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7
Q

What is the structure of somatostatin?

A

14 amino acid cyclic peptide

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8
Q

What is the structure of pancreatic polypeptide?

A

36 amino acid linear polypeptide

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9
Q

What do the A / alpha / alpha 2 cells secrete?

A

Glucagon

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10
Q

What do the B / Beta cells secrete?

A

Insulin

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11
Q

What do the D / alpha 1 / gamma / delta cells secrete?

A

Somatostatin

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12
Q

What do the F cells secrete?

A

Pancreatic polypeptide

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13
Q

What do Epsilon cells produce?

A

Ghrelin (stimulates apetite)

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14
Q

What are the main functions of the endocrine pancreas?

A
  • Control of blood glucose in absorptive state (insulin) and post-absorptive state (glucagon)
  • Stimulate / inhibit digestive enzyme and HCO3- secretion in GI tract (pancreatic peptide and somatostatin)
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15
Q

How many islets of Langerhans are present in the pancreas in humans?

A

~ 1 million - 5 million

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16
Q

What are the majority of the cells in the islet of langerhans?

A

Beta cells

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17
Q

Where are Beta cells generally found in the islet of langerhans?

A

Centre

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18
Q

Where are the alpha cells generally found in the islet of langerhans?

A

Periphery

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19
Q

Where are the delta cells found in the islets of langerhans?

A

Juxtaposed to both alpha and beta cells

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20
Q

How does the blood flow through the islets of langerhans?

A

Through the centre then diffues out to the periphery

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21
Q

What percentage of blood flow to the pancreas goes to the islets of langerhans?

A

10 - 15% (~15 x higher than blood flow to exocrine part)

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22
Q

At what end of mRNA does translation start?

A

5’

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23
Q

What connects the A and B chains of mRNA?

A

2 Disulphide bonds (A folds over to connect with B chain)

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24
Q

What end is the B chain at?

A

Amino terminal end

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25
Q

WHat are the 3 chains of pro-insulin?

A

B, C and A chains (C connects B and A - it is cleaved off to create insulin)

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26
Q

Where is the C chain of pro-insulin cleaved off?

A

Trans-golgi

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27
Q

What reduces the osmotic effect of the secretory granules?

A

Chromatogranins, Zinc

- Create chrystilininsulin zinc complexes

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28
Q

Where are the disulphide bonds found on insulin?

A
  • 2 connect the A and B chains

- 1 is located just on the A chain

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29
Q

What are the factors stimulate insulin release?

A
  • MAINLY Increase in blood glucose
  • Certain amino acids
  • Free fatty acids
  • GI tract hormones (GIP/GLP-1/CCK)
  • Parasympathetic activity (Ach)
  • sympathetic activity (Beta adrenergic)
  • Glucagon (can bind to GLP-1 receptor)
30
Q

What are examples of incretins (GI tract hormones)?

A
  • GIP (gastric inhibitory peptide)
  • GLP-1 (Glucagon-like peptide 1)
  • CCK (cholecystokinin)
31
Q

What factors inhibit insulin release?

A
  • Alpha adrenergic stimulation (NA)
  • Somatostatin
  • Insulin (negative feedback)
32
Q

What transporters facilitate the transport of glucose into Beta cells?

A

GLUT2 transporter

33
Q

Explain the whole mechanism by which insulin is released from pancreatic Beta cells?

A
  • Glucose enters cell via GLUT2 transporter
  • Glucose influx stimulates glycolysis, leads to increase in ATP (or ratio of ATP/ADP inside cell)
  • ATP inhibits ATP-sensitive K+ channel
  • Inhibition of K+ channel causes Vm to become more positive (depolarisation) (K+ does not exit cell)
  • Depolarization activates voltage-gated Ca2+ channel in plasma membrane
  • Ca2+ induced Ca2+ release in endoplasmic reticulum (Ca2+ binds to ryanodine receptors)
  • Elevated Ca2+ leads to exocytosis and release of insulin into the blood within secretory granules
34
Q

What does glucokinase (type of hexokinase) convert glucose into?

A

Glucose-6-phosphate

35
Q

What is the structure of K+ATP channel and what is its function?

A
  • 4 subunits make up channel body
  • 4 subunits which sense ATP ADP etc.
  • Allow K+ to efflux out of cell
  • Closes when high conc of ATP, opens on high concentrations of ADP
36
Q

What kind of receptors are CCK and Ach receptors on the Beta cells - how do they increase insulin release?

A

G-protein coupled - cause IP3 to release Ca2+ from endoplasmic reticulum and Protein kinase C to phsophorylate proteins involved in the exocytosis of insulin

37
Q

What can cause a release of Ca2+ from the endoplasmic reticulum?

A
  • Ryanodine receptors (Ca2+)

- IP3 receptors

38
Q

How do glucagon and Beta adrenergic receptors increase insulin release?

A
  • G-protein coupled
  • Cuases activation of adenylate cyclase - make cAMP
  • Protein kinase A phsodphorylates proteins which augment secretion of insulin
39
Q

How do somatostatins, galanin and alpha-adrenergic agonists decrease insulin release?

A
  • Bind to their own G-protien coupled receptor
  • This interacts with inhibitory G protein which supresses adenylate cyclase and lowers cAMP
  • Some somatostatin receptors can activate K+ ATP channel (hyperpolarisation)
40
Q

How can fatty acids and amino acids increase insulin release?

A

Can be broken down to make ATP

41
Q

What is the physiological action of insulin?

A
  • Increased glycogenesis (Liver, muscle)
  • Increased glucose transport into cells (muscle/ adipose tissue) (GLUT4 transporter recruitment)
  • Decreased blood glucose
  • Increased protein synthesis (binds to insulin receptor and insulin-like growth factor receptors)
  • Increased lipogenesis (liver and adipose tissue)
42
Q

What organ does not increase in glucose permeability as a result of insulin release?

A

Liver (it has GLUT2 transporters) always has glucose permeability

43
Q

What factors stimulate glucagon release?

A

Fasting / absorption of high protein meal in the GI tract - Decreased blood glucose (indirectly)

  • Certain amino acids
  • GI tract hormones (+/-)
  • Parasympathetic stimulation (Ach)
  • Beta adrenergic stimulation (Adrenaline)
  • Alpha adrenergic stimulation (NA)
44
Q

What factors inhibit glucagon release?

A
  • Insulin (Beta cells)
  • Amylin (Beta cells)
    (Paracrine - bind to receptors on Alpha cells)
  • Somatostatin (delta cells)
45
Q

What are the main factors which stimulate glucagon release?

A

Low blood glucose

  • Insulin therefore not released (as K+ channels open to hyperpolarise Beta cells)
  • Insulin and amylin unable to inhibit glucagon
  • Glucagon released
  • Higher centres in the brain also detect low blood glucose -> Nerves and neurotransmitters stimulate glucagon release from alpha cells (through parasympathetic Ach and Adrenaline and NA from Beta and Alpha adrenergic stimulation)
  • Incretins from GI tract may inhibit Delta cellfrom releasing somatostatin - somatostatin cannot inhibit glucagon release
46
Q

How does glucagon increase blood glucose?

A
  • Predominate in liver (also in kidney and heart)
  • No glucagon receptors in adipose tissue
  • Bind to receptors in the liver
  • Increase cAMP
  • Increase glycogenolysis to convert glycogen into glucose 6 phosphate and then glucose which is released into circulation through GLUT2 receptors
  • Increased blood glucose
47
Q

What are the physiological actions of glucagon?

A
  • Increase glycogenolysis -> Increase blood glucose
  • Decreases lipogenesis and increase lipolysis in liver (not adipose) (mainly due to lack of insulin though). Increased free fatty acids and glycerol
  • Increases gluconeogenesis (in presence of cortisol) which increases blood glucose
48
Q

How common in diabetes Mellitus?

A
  • 2 - 3 % of population

- 15 - 20 % in 50 - 60 year olds

49
Q

What is diabetes a result of?

A
  • Insulin deficiency (5 - 10 %)

- Insulin insensitivity (> 90 %)

50
Q

What is the blood glucose concentration in hyperglycaemia in diabetes Mellitus?

A 
> 10 mM
180 mg (mg/dl)
51
Q

What are the effects of hyperglycaemia?

A
  • Glucosuria - tubular fluid exceeds renal threshold for re-absorption
  • Polyuria - osmotic diuresis due to glucose in tubular fluid
  • Polydipsia - due to dehydration increasing angiotensin II levels which acts as dipsogen on thirst centres in brain
  • Increased blood amino acids due to increased protein catabolism
  • Increased blood fatty acids and glycerol due to increased lipolysis in adipose tissue
  • Keto-acidosis - due to incomplete oxidation of fatty acids and ketogenic amino acids
52
Q

What are glucogenic amino acids?

A

Side-chains can be used and inserted into citric acid cycle or glyolytic pathyway and converted back to make glucose

53
Q

What happens to the 4 or 5 amino acids which have side chains which cannot be converted back into TCA cycle intermediates?

A
  • Broken down into acetoacetate or acetone or acetyl CoA
  • Side chains converted into acetyl groups can only used in TCA cycle for respiration or they can form excess acetyl coA - they are ketogenic amino acids
  • Gives an excess of acetyl coA in liver cells
  • Build up of acetoacytate and Beta-OH-butyrate can lose CO2 and create acetone
54
Q

What are the plasma ketones?

A
  • Acetoacytate
  • Beta-OH-butyrate
  • Acetone
55
Q

What is ketonaemia?

A

High levels of ketone bodies in blood

56
Q

What is ketonuria?

A

High levels of ketones in urine

57
Q

How is diabetes Mellitus diagnosed/

A

Glucose tolerance test (> 10 mM 2 hours after glucose challenge)

58
Q

How long does it take for glucose to return to its normal levels after a meal (consumption of glucose)?

59
Q

How long does it take for glucose to reach it’s normal levels in the blood after a meal / consumption of glucose in a diabetic patient?

A

After ~ 5.5 hours it will return to its normal levels, however, these ‘normal’ levels are stil elevated compared to a non-diabetic individual

60
Q

What is the reduction in blood glucose concentration in diabetic patients due to?

A

Mostly the release of glucose in urine - not the uptake of glucose in muscle /adipose by insulin

61
Q

When is the onset of type 1 - insulin-dependent diabetes mellitus usually?

A

Juvenile - onset

62
Q

What is type 1 diabetes mellitus caused by?

A

Destruction of pancreatic Beta cell (auto-immune after viral attack)

63
Q

What virus is thought to often cause the auto-immune reaction in type 1 diabetes mellitus?

A

Coxsackie B virus

64
Q

How is type 1 - insulin dependant diabetes mellitus treated?

A
  • Insulin administration (IM injections of short or long-acting formulations of recombinant insulin)
  • Restricted carbohydrate diet (< 45% of calories in carbohydrates)
65
Q

What is type II - non-insulin dependant diabtes mellitus due to?

A

Capacity of Beta cell to produce insulin decreased / decreased number and affinity of insulin receptors results in reduced insulin responsiveness

66
Q

How is type II diabetes treated?

A
  • Restricted diet (1000 calories / day)
  • Sulphonyl ureas (increased beta cell response to glucose)
  • Biguanides (stimulate glucose uptake in muscle)
  • When uncontrolled - Insulin injection
67
Q

How can glucagon secretion increase in those with type 1 diabetes mellitus?

A
  • Decreased insulin release leds to less inhibition of alpha cells -> Glucagon release
68
Q

What are the primary effects of insulin deficiency

A
  • Increased hepatic glucose output
  • Decreased glucose output by cells
  • Decreased triglyceride synthesis
  • Increased lipolysis
  • Decreased amino acid uptake by cells (increased in blood)
  • Increased protein degradation (increase in amino acids in blood)
69
Q

What are long term effects of diabetes mellitus?

A
  • Increase in fat mobilisation (increase in plasma FFA/TG/Cholesterol)
  • Increase in blood glucose (glycation and glycoxidation of proteins, lipo-proteins, esp LDL)
  • Together causes modification of extracellular structural proteins in arteries and arterioles (deposition of fats in arterial walls) - bulid up of foam cells
  • Damage of vascular endothelium (loss of NO release)
  • Loss of arterial compliance causing diabetic atherosclerosis and hypertension resulting in cardiovascular disease (angina, arrhythmias, renal disease, stokes, diabetic retinopathy, MI)
70
Q

Where does the thymus develop from?

A

The 3rd pharyngeal pouch - migrates inferiorly to the superior mediastinum and loses connection with the pharynx

71
Q

What cells invade and colonise the thymus?

A

Lymphoid thymocytes derived from bone marrow

72
Q

What are the purposes of the thymus?

A
  • Development and education of T lymphocytes

- Secretion of several hormones that promote the maturation of different cells of the immune system

MD4001 Physiology (22 decks)

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