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Endocrine System > The Endocrine Pancreas 1 > Flashcards

The Endocrine Pancreas 1 Flashcards

1
Q

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

A
  • Feeding Centre - promotes feelings of hunger and drive to eat
  • Satiety Centre – promotes feelings of fullness by suppressing the Feeding Centre
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2
Q

What controls activity in the Feeding and Satiety Centres?

A

A complex balance of neural and chemical signals as well as the presence of nutrients in plasma

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3
Q

Define 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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4
Q

Define the Lipostatic theory

A

Food intake is determined by fat stores: as fat stores increase, the drive to eat decreases (- feeding centre; + Satiety Centre).
• Leptin release

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5
Q

What is leptin?

A

A peptide hormone released by fat stores which depresses feeding activity.

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6
Q

What occurs in the disruption of the Glucostatic and Lipostatic theory pathways?

A
  • Obesity

* Type I DM can present with hunger despite eating as no satiety centra stimuli as less insulin

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7
Q

Name the three categories of energy output

A
  • Cellular work
  • Mechanical work
  • Heat loss
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8
Q

What is cellular work?

A

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

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9
Q

What is mechanical work?

A

Movement, either on large scale using muscle or intracellularly.

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10
Q

What is heat loss?

A

Associated with cellular and mechanical work accounts for half our energy output.

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11
Q

What are the three elements of metabolism?

A
  1. Extracting energy from nutrients in food (digestion)
  2. Storing that energy (anabolic process)
  3. Utilising that energy for work (catabolic process)
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12
Q

What state does the body enter after eating?

A

Absorptive state

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13
Q

Define the absorptive state

A

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

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14
Q

What state does the body enter between meals and overnight?

A

Post-absorptive state

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15
Q

Define the post-absorptive state

A

The pool of nutrients in the plasma decreases and we enter 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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16
Q

What occurs in catabolic pathways?

A

Break Down. Net effect is degradation of large molecules into smaller ones, releasing energy for work.

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17
Q

What occurs in anabolic pathways?

A

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

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18
Q

Why does the brain have top priority of accessing glucose?

A

Most cells can use fats, carbohydrates or protein for energy but the brain can only use glucose (except in extreme starvation uses ketone bodies), 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 occurs if [BG] is not sufficient for the brain?

A

hypoglycaemia which can lead to coma and death

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20
Q

Through what two processes is [BG] maintained?

A

By synthesising glucose from glycogen (glycogenolysis) or amino acids (gluconeogensis)

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21
Q

What occurs to BG in diabetes?

A

Glc cannot be taken up so BG rises and glucose is detected in the urine

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22
Q

What is the normal range of [BG]?

A

4.2 - 6.3mM

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23
Q

What is the range of hypoglycaemia?

A

[BG] < 3mM

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24
Q

What to endocrine hormones produced by the pancreas maintain [BG]?

A

Insulin and glucagon

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25
Q

Describe the secretions produced by 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.

26
Q

What are the four cells in the Islet of Langerhans and what do they produce?

A
  • Alpha cells -> glucagon
  • Beta cells -> insulin
  • Delta cells -> somatostatin
  • F cells -> pancreatic polypeptide (unknown function)
27
Q

What do alpha cells produce?

A

Glucagon

28
Q

What do B cells produce?

A

Insulin

29
Q

What do delta cells produce?

A

Somatostatin

30
Q

What do F cells produce?

A

Pancreatic polypeptide

31
Q

What does the control of Blood glucose depend on?

A

Balance between insulin and glucagon

32
Q

What occurs if insulin dominates over glucagon?

A 
Increase in:
• Glucose oxidation 
• Glycogen synthesis 
• Fat synthesis 
• Protein synthesis

Glucose taken up be cells from plasma ([BG] decreases)

33
Q

What occurs if glucagon dominate over insulin?

A

Increase in:
• Glycogenolysis
• Gluconeogenesis
• Ketogenesis

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

34
Q

Define glycogenolysis

A

Breakdown of glycogen

35
Q

Define gluconeogenesis

A

Generation of glucose

36
Q

What is insulin?

A

Peptide hormone produced by pancreatic B cells. Stimulates glucose uptake by cells.

37
Q

Describe formation of insulin

A
  1. Synthesized as a large preprohormone, preproinsulin, which is then converted to proinsulin in the ER.
  2. Proinsulin is then packaged as granules in secretory vesicles.
  3. Within the granules the proinsulin is cleaved again to give insulin and C-peptide.
  4. Insulin is stored in this form until the cell is activated and secretion occurs.
38
Q

What stimulates insulin release?

A

Plasma glucose and amino acids

39
Q

What is the only hormone which would lower [BG]?

A

Insulin

40
Q

What occurs to glucose during the absorptive state?

A

Utilised by cells as their energy source, and any excess is stored as glycogen in liver and muscle, and as triacylglycerols (TAG) in liver and adipose tissue.

41
Q

What happens to amino acids during the absorptive state?

A

Used mainly to make new proteins with excess being converted to fat. Also form an energy source.

42
Q

What happens to fatty acids during the absorptive state?

A

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

43
Q

Describe the mechanism of control of insulin secretion by [BG]

A

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

  1. When glucose is abundant it enters cells through glucose transport proteins (GLUT) and metabolism increases.
  2. This increases [ATP] within the cell causing the K-ATP channel to close.
  3. Intracellular [K+ ] rises, depolarising the cell.
  4. Voltage-dependent Ca2+ channels open and trigger insulin vesicle exocytosis into the circulation.
44
Q

What is the primary action of insulin?

A

Binds to tyrosine kinase receptors on the cell membrane of insulin-sensitive tissues (muscle and adipose tissue) to increase glucose uptake by these tissues.

45
Q

How does insulin effect Glc uptake by muscle and adipose tissue?

A

These tissue can only take up glucose when insulin is present

Insulin stimulates the mobilisation of specific glucose transporters, GLUT-4, which reside in the cytoplasm of unstimulated muscle and adipose cells.

46
Q

How does insulin increase uptake of Glc by adipose and muscle tissue?

A

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.

47
Q

Describe the steps in insulins role in Glc uptake in muscle and adipose tissue

A
  1. Insulin binds to receptor
  2. Signal transduction cascade
  3. Exocytosis of GLUT4 to apical membrane
  4. Glucose enters cell
48
Q

Do all tissues require insulin to take up glucose?

A

Not, only muscle and fat (but they make up large proportion of body)

49
Q

Name three GLUT-transporters which are not insulin-dependent

A
  • GLUT-1 - Basal glucose uptake in many tissues eg brain, kidney and red blood cells.
  • GLUT-3 - Similar • GLUT-2 - cells of pancreas and liver
50
Q

What GLUT-transporter is dependent on insulin?

A

GLUT-4 in muscle and fat

51
Q

How does the liver take up glucose?

A

The liver is not an insulin-sensitive tissue. Liver takes up glucose by GLUT 2 transporters, which are insulin independent.

Glucose enters down concentration gradient.

52
Q

Does insulin effect Glc uptake by hepatocytes?

A

Although insulin has no direct effect on the liver, glucose transport into hepatocytes is affected by insulin status.

53
Q

How does insulin effect Glc uptake by hepatocytes in the fed state?

A

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

54
Q

How does insulin effect Glc uptake by hepatocytes in the 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.

Less insulin due to no glucose in plasma means [Glc]ic is higher than blood

55
Q

Name seven additional actions of insulin

A

Anabolic processes:
• Increases glycogen synthesis in muscle and liver.
• 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 (See GH Lecture)
  • Promotes K+ ion entry into cells by stimulating Na+/K+ ATPase. Very important clinically.
56
Q

How does insulin increase glycogen synthesis in muscle and liver?

A

Stimulates glycogen synthase and inhibits glycogen phosphorylase

57
Q

What happens to insulin once its action is complete?

A

Insulin-bound receptors are internalised by endocytosis and destroyed by insulin protease, some recycled.

58
Q

Name five stimuli which increase 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 eg gastrin, secretin, CCK, GLP-1, GIP.
  • Vagal nerve activity
59
Q

Why do incretin hormones controlling GI secretion and motility stimulate insulin release?

A

Released by ileum and jejunem in response to nutrients. Early insulin release prevents glucose surge when absorption occurs.

60
Q

Why does glucagon stimulate insulin secretion?

A

As glucagon increases blood glucose but insulin needed to muscle and adipose tissue to uptake glucose

61
Q

How does vagal stimulation increase insulin release?

A

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

As IV Glc means it doesn’t need to be absorbed by GI tract, so less hormones are released so less insulin than if Glc ingested orally.

i.v. glucose –> increase insulin by direct effect of increase glucose on B cells.

But even more insulin released if vagal activity stimulated:

Oral loading of same amount of glucose –> increase insulin by both direct effect on B cells and vagal stimulation of B cells, plus incretin effects!

Endocrine System (29 decks)

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