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Endocrine system > The Endocrine Pancreas > Flashcards

The Endocrine Pancreas Flashcards

1
Q

Define what an obligatory glucose utilising tissue is and give an example

A

Refers to a tissue that can only utilise glucose in energy production e.g. brain (though it can adapt to use ketones in periods of starvation)

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2
Q

Describe the glucostatic theory

A

Glucostatic theory – food intake is determined by blood glucose: as [BG] increases, the drive to eat decreases (- Feeding Centre; + Satiety centre)

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3
Q

Describe the lipostatic theory

A

Lipostatic theory – food intake is determined by fat stores: as fat stores increase, the drive to eat decreases (- feeding centre; + Satiety Centre).

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4
Q

What peptide hormone is released to depress feeding activity?

A

Leptin

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5
Q

What are the 3 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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6
Q

What are the three elements of metabolism?

A

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

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7
Q

Describe anabolic pathways

A

Anabolic pathways = Build Up. Net effect is synthesis of large molecules from smaller ones, usually for storage purposes. Requires energy. E.g. absorptive phase post feeding

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8
Q

Describe catabolic pathways

A

Catabolic pathways = Break Down. Net effect is degradation of large molecules into smaller ones, releasing energy for work. E.g. post absorptive/fasted state

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9
Q

What is the normal [blood glucose]?

A

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

5 mmoles useful to remember

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10
Q

At what [blood glucose] are individuals hypoglycaemic?

A

Hypoglycaemia = [BG] < 3mM

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11
Q

What two hormones are directly involved in blood glucose concentration control?

A

Insulin and glucagon

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12
Q

What % of the pancreas acts as an exocrine gland, and what does it produce?

A

99%

Releases enzymes and sodium bicarbonate into GI tract

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13
Q

What % of the pancreas acts as an endocrine gland, and what does it produce?

A

1% (islets of langerhans)

α (alpha) cells produce glucagon
β (beta) cells produce insulin
δ (delta) cells produce somatostatin
F cells produce pancreatic polypeptide (function not really known, may help control of nutrient absorption from GIT

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14
Q

What 4 endocrine hormones does the pancreas make?

A

Glucagon
Insulin
Somatostatin
Pancreatic polypeptide

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15
Q

What cells in the islets of langerhans produce glucagon?

A

Alpha cells (α)

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16
Q

What cells in the islets of langerhans produce insulin?

A

β (beta) cells

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17
Q

What cells in the islets of langerhans produce somatostatin?

A

δ (delta) cells

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18
Q

What cells in the islets of langerhans produce pancreatic polypeptide?

A

F cells

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19
Q

What type of hormone is insulin and what is its primary action?

A

Peptide endocrine hormone which stimulates glucose uptake by muscle and adipose tissues (insulin-sensitive tissues)

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20
Q

Where is the preprohormone preproinsulin converted to prohormone proinsulin?

A

Endoplasmic reticulum following synthesis

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21
Q

Where is the prohormone proinsulin converted to active insulin alongside C peptide?

A

In the secretory vesicles when it is packaged alongside proteolytic enzymes

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22
Q

What stimulates insulin secretion?

A

Increased blood glucose and blood amino acid levels following feeding during absorptive phase

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23
Q

How is excess glucose stored?

A

Any excess glucose is stored as :

  • glycogen in liver and muscle
  • triacylglycerols (TAG) in liver and adipose tissue
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24
Q

How is excess amino acids stored?

A

Used to create proteins

Excess is stored as fat

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25
Q

How are fatty acids stored?

A

Fatty acids are stored in the form of triglycerides in adipose tissue and liver.

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26
Q

How does increased blood glucose cause the secretion of insulin?

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.

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27
Q

Which glucose transporter is mobilised by insulin, and where is it found?

A

GLUT-4 - when insulin is present, it moves to the membrane of cells to allow for glucose entry into cells

Found on insulin sensitive tissues e.g. adipose and resting muscle tissues. Most tissues do not require insulin for glucose absorption

When insulin is removed, GLUT4 return to cytoplasm

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28
Q

What % of BW in normality of the human body is made up of fat and muscle?

A

Muscle is ≈ 40% BW and fat ≈ 20-25% of BW

Large proportion of human body is insulin sensitive

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29
Q

What are the 3 other GLUT transporters not reliant on insulin for glucose transport, and where are they found?

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

30
Q

What GLUT transporter is found on beta cells of the pancreas and liver?

A

GLUT-2

31
Q

How does insulin indirectly alter glucose uptake in liver hepatocytes?

A

In fed state, liver takes up glucose via GLUT2 because liver hexokinase is activated by insulin, causing a drop in intracellular [BG], creating a gradient of glucose to draw it into cells.
In fasted state, liver synthesises glucose causing an increase in IC [glucose], creating a gradient favouring movement of glucose out of cells

32
Q

What are the 7 additional actions of insulin?

A

Increases glycogen synthesis in muscle and liver.

Stimulates glycogen synthase and inhibits glycogen phosphorylase (used in glycogenolysis)

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

Has a permissive effect on Growth Hormone

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

33
Q

What hormone causes a permissive effect on growth hormone?

A

Insulin

34
Q

What is the half life of insulin in plasma, and where is it degraded?

A

Insulin has a half-life of ≈ 5 minutes and is degraded principally in the liver and kidneys.

35
Q

What degrades insulin and its receptors?

A

Insulin protease following endocytosis of bound receptors

36
Q

What kind of receptor is the insulin receptor?

A

Tyrosine kinase receptor

37
Q

What stimuli increases insulin release?

A
  • Increased [BG]
  • 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 e.g. gastrin, secretin, CCK, GLP-1, GIP. Released by ileum and jejunem in response to nutrients. Early insulin release prevents glucose surge when absorption occurs
  • Vagal nerve activity
38
Q

What stimuli inhibits insulin release?

A
  • Low [BG]
  • Somatostatin (GHIH)
  • Sympathetic α2 effects
  • Stress e.g. hypoxia
39
Q

What type of hormone is glucagon, where is it produced and what is its primary action?

A

Peptide hormone produced by α-cells of the pancreatic islet cells

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

40
Q

On what organ does glucagon mainly act on?

A

Liver (mobilises glucose from stores and creates it from various substrates)

41
Q

What is the half life of glucagon in plasma, and where is it degraded?

A

Plasma half-life 5-10mins, degraded mainly by liver.

42
Q

What 4 hormones are involved in the glucose counter-regulatory control system?

A

Glucagon
Epinephrine
Cortisol
GH

43
Q

When is glucagon most active?

A

Post-absorptive phase (fasting)

44
Q

What type of receptors are glucagon receptors?

A

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

45
Q

What occurs following glucagon receptor activation?

A

Glucagon receptors are G-protein coupled receptors linked to the adenylate cyclase/cAMP system which when activated phosphorylate specific LIVER enzymes resulting in:

  • Increased glycogenolysis
  • Increased gluconeogenesis (from aa’s and glycerol)
  • Formation of ketones from fatty acids (from lipolysis)
46
Q

How are ketones produced for formation of fatty acids in states of low energy?

A

Ketones are made from fatty acids obtained from lipolysis

47
Q

How is glycerol produced for gluconeogenesis in states of low energy?

A

Glycerol is obtained from lipolysis

48
Q

At what [blood glucose] is glucagon secretion dramatically increased?

A

Glucagon release is relatively constant although secretion increases dramatically when [BG] < 5.6mM

49
Q

What hormones are secreted in response to increased amino acid concentrations in the blood?

A

Insulin and glucagon

Prevents dramatically low glucose levels (glucose sparing for the brain) following high protein meals with low carb intake (typical carnivore diet)

50
Q

What stimuli promotes glucagon release?

A
  1. Low [BG]
  2. High [amino acids]. Prevents hypoglycaemia following insulin release in response to aa.
  3. Sympathetic innervation and epinephrine, β2 effect
  4. Cortisol
  5. Stress e.g. exercise, infection
51
Q

What stimuli inhibits glucagon release?

A
  1. Glucose
  2. Free fatty acids (FFA) and ketones
  3. Insulin (fails in diabetes so glucagon levels rise despite high [BG] )
  4. Somatostatin
52
Q

What is the result of parasympathetic innervation of islet cells?

A

↑ Parasympathetic activity (vagus) →↑ insulin and to a lesser extent ↑ glucagon, in association with the anticipatory phase of digestion.

53
Q

What is the result of sympathetic innervation of islet cells?

A

↑ Sympathetic activation promotes glucose mobilization →↑ glucagon, ↑ epinephrine and inhibition of insulin, all appropriate for fight or flight response.

54
Q

What type of hormone is somatostatin, where is it produced and what is its primary action?

A

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

Main pancreatic action is to inhibit activity in the GI Tract. Function appears to be to slow down absorption of nutrients to prevent exaggerated peaks in plasma concentration

55
Q

How could synthetic somatostatin be used clinically?

A

Synthetic SS may be used clinically to help patients with life-threatening diarrhoea associated with gut or pancreatic tumours

56
Q

How does somatostatin affect insulin and glucagon?

A

SS is NOT a counter-regulatory hormone in the control of blood glucose but it does strongly suppress the release of both insulin and glucagon in a paracrine fashion.

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

57
Q

What affect does exercise have on [blood glucose]?

A

The entry of glucose into skeletal muscle is increased during exercise, even in the absence of insulin.

Exercise also increases the insulin sensitivity of muscle, and causes an insulin-independent ↑ in the number of GLUT-4 transporters on active muscle cells incorporated into the muscle membrane.

This effect persists for several hours after exercise and regular exercise can produce prolonged increases in insulin sensitivity.

58
Q

How are ketone bodies produced?

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 the liver will convert excess FFAs to ketone bodies, which provides an additional source for muscle and brain

Important - After a period of starvation, the brain adapts to be able to use ketones.

59
Q

What % of patients are insulin dependent?

A

10%

60
Q

Describe the aetiology of type 1 DM

A

Autoimmune destruction of the pancreatic β-cells destroys ability to produce insulin and seriously compromises patient’s ability to absorb glucose from the plasma.
Untreated type 1 diabetes leads to many complex changes in the body, which ultimately cause starvation and death.

61
Q

What is ketoacidosis?

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

However, in poorly controlled insulin-dependent diabetes, a lack of insulin depresses ketone body uptake. They build up rapidly in the plasma and because they are acidic create life threatening acidosis (ketoacidosis or ketosis) with plasma pH < 7.1. Death will occur within hours if untreated.

Ketones detectable in urine and produce distinctive acetone smell to breath.

62
Q

What causes insulin resistance in normally insulin sensitive tissues in type 2 DM?

A

Muscle and fat no longer respond to normal levels of insulin. This is either due to an abnormal response of insulin receptors in these tissues or a reduction in their number.

63
Q

What % of DM patients are insulin-resistant?

A

90% of diabetic patients are insulin-resistant (NIDDM)

64
Q

How is type II DM/NIDDM treated?

A

Initial treatment is aimed at trying to restore insulin sensitivity of tissues with exercise and dietary change. If caught at pre-diabetic stage can prevent progression to full blown diabetes. If this fails, oral hypoglycaemic drugs will be used

Metformin is the first line treatment, which inhibits hepatic gluconeogenesis and antagonises action of glucagon

Sulphonylureas are a class of drug which act to close the KATP in β cells and ∴stimulate Ca2+ entry and insulin secretion.

Low level insulin to prevent hyperglycaemia

65
Q

What is the mechanism of action of metformin?

A

Metformin is the first line treatment, which inhibits hepatic gluconeogenesis and antagonises action of glucagon

66
Q

What is the mechanism of action of sulphonylureas?

A

Sulphonylureas are a class of drug which act to close the KATP channels in β cells and ∴stimulate Ca2+ entry and insulin secretion.

67
Q

What is the first line of hypoglycaemic drugs used for type II DM?

A

Metformin

68
Q

What is the diagnostic criterion for diabetes and how is it tested?

A

Hyperglycaemia (elevated [BG]) is the diagnostic criterion for diabetes. Detected by performing a “Glucose Tolerance Test”

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.

Does not distinguish Type I from II

69
Q

What diabetic complications are associated with hyperglycaemia?

A

o Retinopathy
o Neuropathy
o Nephropathy
o Cardiovascular Disease

70
Q

What diabetic complications are associated with hypoglycaemia?

A

o 4.6mM [BG] → inhibition of insulin secretion
o 3.8mM [BG] → glucagon, epinephrine and GH secretion
o 3.2mM [BG] → cortisol secreted
o 2.8mm [BG] → cognitive dysfunction
o 2.2mM [BG] → lethargy
o 1.7mM [BG] → coma
o 1.1mM [BG] → convulsions
o 0.6mM [BG] → permanent brain damage and death

71
Q

What type of diabetic patients are at risk of hyperglycaemia?

A

Type II and type II DM

72
Q

What type of diabetic patients are at risk of hypoglycaemia?

A

Primarily type I DM patients on exogenous insulin

Endocrine system (27 decks)

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