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Endocrine System > The Endocrine Pancreas 2 > Flashcards

The Endocrine Pancreas 2 Flashcards

1
Q

What is glucagon?

A

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

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2
Q

What is the function of glucagon?

A

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

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3
Q

What is the plasma half life of glucagon?

A

5-10mins, and degraded mainly by the liver.

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4
Q

What hormones are involved in the glucose counter-regulatory control system (opposing action of insulin)?

A
  • Glucagon
  • Epinephrine
  • Cortisol
  • GH
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5
Q

What is the action of glucagon

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 (substrates: AA and glycerol (lipolysis))
  • Formation of kenos from FA (lipolysis)

All occur in the liver and net result elevated [BG]

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6
Q

Describe the steps in how glucagon elevates [BG]

A
  1. Liver glycogen becomes glucose
  2. Adipose lipids become free FA and glycerol that enter blood
  3. Muscle glycogen can be used for energy. Also uses FA and break down their proteins to AA that enter blood
  4. Brain can use only glucose and ketones for energy
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7
Q

At what level of [BG] does glucagon increase dramatically?

A

< 5.6 mM

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8
Q

Why are amino acids potent stimulus for glucagon secretion? And what would happen if they weren’t?

A

AA stimulates to release of insulin, for anabolic process to store away
Whilst it does this it removes glucose from plasma
Therefore, glucagon released to maintain blood glucose, if not, would cause hypoglycaemia

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9
Q

What do amino acids in the plasma stimulate in the release of?

A

Insulin and glucagon.

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

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10
Q

Why is there extra glucose in the post-absorptive state for the brain?

A

Lower insulin levels mean a large mass of tissue, i.e. muscle and fat, cannot readily access glucose and so there is glucose sparing for obligatory glucose users.

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11
Q

Name five stimuli that promote glucagon release

A
  • Low [BG]
  • High [amino acids] - prevents hypoglycaemia following insulin release in response to AA
  • Sympathetic innervation and epinephrine, B2 effect
  • Cortisol
  • Stress e.g. exercise, infection

Last 3 ensures adequate amount of glucose in the plasma at time of stress to maintain the brain

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12
Q

Name four stimuli that inhibit glucagon release

A
  • Glucose
  • FFA and ketones
  • Insulin (fails in diabetes so glucagon levels rise despite high [BG] )
  • Somatostatin
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13
Q

What is the effect of increased parasympathetic activity?

A

In the anticipatory phase of digestion:
• Increased Insulin
• Lesser extent increase in glucagon (to balance action of insulin to ensure Glc in blood for brain)

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14
Q

What is the effect of increased sympathetic activity?

A

Fight or flight response:
• Increase glucagon
• Increase epinephrine
• Inhibition of insulin

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15
Q

What is GH?

A

It is an antagonist of insulin by removing some of the receptor on muscle and adipose tissue, desensitising tissue to it

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16
Q

What is the action of epinephrine?

A
  • Muscle glycogenolysis
  • Liver glycogenolysis
  • Gluconeogenesis
  • Lipolysis
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17
Q

What is the action of cortisol?

A
  • Gluconeogenesis
  • Inhibition of glucose uptake
  • Lipolysis
  • Protein catabolism
18
Q

What is the action of GH?

A
  • Gluconeogenesis
  • Inhibition of glucose uptake
  • Lipolysis
19
Q

What is somatostatin?

A

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

20
Q

What is the action of somatostatin?

A

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 concentrations.

It is NOT a counter regulatory hormone but does inhibit release of insulin and glucagon.

Aka GHIH inhibits secretion of GH from anterior pituitary

21
Q

What do patient with somatostatin-secreting tumour present with?

A

Develop symptoms of diabetes which disappear when when tumour is removed

22
Q

What stimulates somatostatin release?

A

Elevated plasma [AA] and [BG]

23
Q

What is the effect of exercise on [BG]?

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 increase in the number of GLUT-4 transporters incorporated into the muscle membrane.

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

24
Q

What is utilised for energy during periods of starvation?

A

FFA from adipose tissue can be used by most tissues and liver will convert excess FFA to ketone bodies, which provides an additional source for muscle and brain.

This is to spare protein from being broken down excessively (would be very weakening, vulnerable to infection) - it is a last resort

25
Q

What happens to the brain after a period of starvation?

A

Adapts to be able to use ketones

26
Q

What occurs in Type I DM?

A

Autoimmune destruction of the pancreatic B-cells destroys ability to produce insulin and seriously compromises patients ability to absorb glucose from the plasma.

27
Q

What occurs if Type I DM (IDDM) is untreated?

A

Type I patients have an absolute need for insulin, without it they become excessively wasted, develop ketoacidosis, coma and die.

28
Q

How is the homeostatic control of BG affected in diabetes?

A
  1. Meal
  2. Increase [BG]
  3. Glucose not taken up by cells due to lack of insulin produced by B cells
  4. Liver still produces glucose
  5. Elevation in [BG]
29
Q

How does ketoacidosis occur in Type I DM?

A

In starvation, FFA can be used to produce energy and the liver will convert excess to ketone bodies for the muscle and brain.

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. Death will occur within hours if untreated.

30
Q

What are signs of ketoacidosis?

A

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

31
Q

What happens in Type II Diabetes (NIDDM)?

A

Peripheral tissues become insensitive to insulin = insulin resistance. 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.

B-cells remain intact and appear normal, there may even be hyperinsulinaemia.

32
Q

How can insulin desensitisation occur in NIDDM?

A

Chronic exposure to high levels of insulin due to high levels of sugar, so tissue become desensitised to insulin as they decrease in numbers of receptors

33
Q

What is the aim of treatment in NIDDM?

A

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)

34
Q

What drugs are used to treat Type II DM (NIDDM)?

A

Oral hypoglycaemic drugs
• Metformin
• Sulphonylureas

Eventually many type II patients end up taking insulin in order to prevent hyperglycaemia

35
Q

What is the action of metformin in NIDDM?

A

Inhibits hepatic gluconeogenesis and antagonises action of glucagon

36
Q

What is the action of sulphonylureas in NIDDM?

A

Act to close the KATP in cells and therefore stimulate Ca2+ entry and insulin secretion.

Obviously requires functioning B cells, so cannot be used in IDDM

37
Q

What is the diagnostic criterion for diabetes?

A

Hyperglycaemia as it occurs in both but for different reasons

38
Q

How is hyperglycaemia detected in diabetes?

A

Glucose tolerance test

39
Q

Describe the glucose tolerance test

A

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

40
Q

What conditions can arise after prolonged hyperglycaemia?

A
  • Retinopathy
  • Neuropathy
  • Nephropathy
  • Cardiovascular Disease

Endocrine System (29 decks)

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