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Year 2 - Endocrine > Endocrine pancreas 1 + 2 > Flashcards

Endocrine pancreas 1 + 2 Flashcards

1
Q

Define the term obligatory glucose utiliser and give an example of this

A

= can only meet its energy demands from glucose and no alternative source, i.e. BRAIN

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2
Q

State the range of plasma glucose that may be expected in normal resting subjects who have fasted overnight

A

4.2-6.3mM (80-120mg/dl)

average 5mM

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3
Q

Describe the process by which insulin is released

A

Released when there’s high BG (main stimulus), although amino acids in blood can also stimulate its release

Beta 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 –> triggers voltage-dependent Ca2+ channels to open and subsequently insulin vesicle exocytosis into the circulation

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4
Q

Energy (food) intake is determined by the balance of activity in what 2 hypothalamic centres

A

Feeding centre - promotes feelings of hunger

Satiety centre - promotes feelings of fullness

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5
Q

Describe the glucostatic theory

A

as [BG] increases, the drive to eat decreases

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6
Q

Describe the lipostatic theory + what hormone suppress feeding

A

as fat stores increase, the drive to eat decreases

Leptin, a peptide hormone released by fat stores, depresses feeding activity

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7
Q

What are anabolic pathways

A

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

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8
Q

What are catabolic pathways

A

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

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9
Q

After eating we enter an Absorptive State where ingested nutrients supply the energy needs of the body and excess is stored

Is this a catabolic or anabolic phase

A

anabolic

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10
Q

Between meals and overnight, 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

Is this a catabolic or anabolic phase

A

catabolic

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11
Q

Most cells can use fats, carbohydrates or protein for energy but the brain can only use … except when…

A

glucose

except in extreme starvation – use ketones

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12
Q

When no new carbohydrate is gained by the body we MUST still maintain blood glucose concentration [BG] sufficient to meet the brain’s requirements

2 ways this can be done:

A

synthesising glucose from glycogen (glycogenolysis) or amino acids (gluconeogenesis)

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13
Q

Hypoglycaemia when [BG] is

A

3mM or less

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14
Q

Lipogenesis (converting glucose to fat) and glycogenesis (converting glucose to glycogen) are stimulated by what hormone + why

A

Insulin

they are processes that uptake glucose

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15
Q

Glycogenolysis + gluconeogenesis are stimulated by what hormone + why

A

Glucagon

They are processes that produce glucose which is what glucagon wants (to raise BG)

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16
Q

What percentage of the pancreas has an endocrine function

A

1%

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17
Q

4 types of islet cells (making up islets of langerhans)

A

alpha
beta
delta
F

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18
Q

What do the following islet cells produce

  • alpha
  • beta
  • delta
  • F
A

glucagon

insulin

somatostatin (GHIH)

pancreatic polypeptide

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19
Q

Excess glucose is stored as what 2 things (2)

A

glycogen in liver and muscle

triacylglycerols (TAG) in liver and adipose tissue

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20
Q

What is the only hormone that lowers [BG]

A

Insulin

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21
Q

How are fatty acids stored

A

as triglycerides in adipose tissue and liver

22
Q

How is insulin synthesised (4)

A

Synthesized as a large preprohormone (preproinsulin) which is then converted to proinsulin in the ER

Proinsulin is then packaged as granules in secretory vesicles with proteolytic enzymes

Within the granules the proinsulin is cleaved again to give insulin and C-peptide

Insulin is stored in this form until the beta cell is activated and secretion occurs

23
Q

Sites of action of insulin (2)

A

Muscle
+
Adipose
tissue

24
Q

Mechanism of action of insulin on BG levels (2)

  • what receptors does it bind to
  • what is mobilised to cell membrane
A

Binds to tyrosine kinase receptors on the cell membrane of insulin-sensitive tissues (muscle and adipose tissue)

Stimulates GLUT-4 transporters which reside in the cytoplasm to migrate to the membrane in order to let glucose into the cell and so decrease BG

25
Q

Some cells are insulin sensitive but not insulin dependent, what tissues are insulin dependent (2)

A

Skeletal muscle + adipose tissue

26
Q

Is the liver insulin sensitive

A

No

27
Q

How does the liver uptake glucose

-what transporters are involved

A

by GLUT 2 transporters, which are insulin independent.

Glucose enters down concentration gradient

28
Q

Although the liver is not insulin sensitive (i.e. insulin has no direct effect on liver), glucose transport in and out hepatocytes is still INDIRECTLY affected by insulin status in order to maintain BG

Describe this indirect effect of insulin status on glucose transport in/out of hepatocytes when

  • plasma insulin is high
  • plasma insulin is low
A

When BG is high so HIGH insulin, insulin activates hexokinase which lowers [glucose] intracellularly, creating a gradient favouring glucose movement into the cells

When BG is low so LOW insulin, liver synthesises glucose via glycogenolysis and gluconeogenesis, increasing [glucose] intracellularly creating a gradient favouring glucose movement out of the cells

29
Q

As well as insulin decreasing [BG], what additional actions does it have (6)

A

Increases glycogen synthesis in muscle and liver by stimulating glycogen synthase and inhibits glycogen phosphorylase

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

Inhibits gluconeogenesis in the liver (to stop more glucose production)

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

30
Q

Insulin half life

A

around 5 mins

-short like all peptide hormones

31
Q

Stimuli which promote insulin release (5)

A

Increased [BG]

Increased [amino acids] in plasma

Glucagon (indirectly; as glucagon stimulates gluconeogenesis which creates glucose so then insulin would be needed to take up the glucose produced)

Other hormones controlling GI secretion/motility, e.g. gastrin, secretin

Vagus nerve activity

32
Q

Stimuli which inhibit insulin release (4)

A

Low [BG]
Somatostatin (GHIH)
Sympathetic a2 receptor effects - lower BP
Stress, e.g. hypoxia

33
Q

Is the insulin response to an IV glucose load the same as that to an oral loading of the same amount of glucose

A

No because oral glucose also stimulates the vagus nerve which stimulates B cells to release insulin as well as release of GI hormones that trigger digestive processes so oral glucose stimulates B cells twice (by direct effect of increased glucose on B cells and vagal stimulation of B cells)

whereas IV glucose just stimulates insulin release due to the effect of increased glucose on B cells

34
Q

Primary function of glucagon + what organ does it mainly act on

A

Raise [BG]

liver

35
Q

What are the counter regulatory hormones of glucose (i.e. the 4 [BG] raising hormones) (4)

A

glucagon, adrenaline/epinephrine, cortisol, GH

36
Q

Glucagon is most active in the absorptive or post-absorptive state

A

post-absorptive

-as glucose has been absorbed so now need more glucose back in blood

37
Q

Mechanism of action of glucagon on raising BG levels

  • what receptor does it bind to + where is this receptor
  • once its receptor is activated, what 3 processes are stimulated to raise to produce glucose and raised BG
A

Glucagon binds to its G-protein coupled receptors (on liver) linked to the adenylate cyclase/cAMP system which when activated, phosphorylate specific liver enzymes, resulting in:

  1. increased glycogenolysis (to put glucose in blood)
  2. increased gluconeogenesis (to put glucose in blood)
  3. formation of ketones from fatty acids (for brain and peripheral tissues)
38
Q

When glucose drops below what level does glucagon release increase dramatically

A

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

39
Q

What stimuli is common between insulin and glucagon release (i.e. stimulates them both to be released)

+ why is it important for both to be released in response to this stimuli

A

Amino acids in plasma

  • esp important for both to be released after a HIGH PROTEIN, LOW CARB MEAL
  • as amino acids are a stimuli of insulin, after a protein rich meal, insulin would cause glucose uptake leading to a lowered BG
  • however if it weren’t for the effect of amino acids on glucagon as well then the insulin stimulating effects of amino acids would result in a very low BG in the case of a HIGH PROTEIN, LOW CARB MEAL as that wouldn’t provide much glucose in the first place
40
Q

Stimuli that promote glucagon release (5)

A

Low BG
High plasma amino acid conc. (also a stimuli of insulin release)
Sympathetic innervation & epinephrine, b2 effects
Cortisol
Stress, e.g. exercise, infection

41
Q

Stimuli that inhibit glucagon release (4)

A

High BG
Free fatty acids & ketones
Insulin
Somatostatin (GHIH)

42
Q

How does autonomic (sympathetic/parasympathetic) activity influence release of insulin/glucagon

  • sympathetic
  • parasympathetic
A

Increased sympathetic activation promotes glucose mobilization –> increased glucagon, increased epinephrine and inhibition of insulin, all appropriate for fight or flight response

Increased parasympathetic activity (vagus) –> increased insulin and to a lesser extent increased glucagon, in association with the anticipatory phase of digestion

43
Q

Somatostatin is a peptide hormone secreted by what 2 things

A

Delta cells of the pancreas

Hypothalamus

44
Q

Main pancreatic function of somatostatin (GHIH)

+ other functions (2)

A

Inhibit GI tract activity
-to slow down nutrient absorption

Suppresses the release of insulin and glucagon in a paracrine fashion, but isn’t a counter-regulatory hormone in the control of BG

Inhibits secretion of GH from AP

45
Q

Describe how glucose metabolism can change in times of stress (exercise, starvation, diabetes)
- talk about exercise specifically

A

Exercise increases insulin sensitivity of muscle and causes an insulin INDEPENDENT increase in GLUT4 transporters recruited to the membrane (i.e. transporters are recruited even if insulin is absent so exercise causes glucose uptake independent of insulin)

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

46
Q

Describe how glucose metabolism can change in times of stress (exercise, starvation, diabetes)
- talk about starvation specifically

A

When nutrients are scarce, body relies on stores for energy, i.e. adipose tissue is broken down, fatty acids + glycerol are released

Free fatty acids readily used by most tissues as energy and liver will convert excess fatty acids to ketone bodies to provide additional energy for muscle & brain

Brain adapts to use ketones after a while of starvation which allows protein to be SPARED instead of being broken down into gluconeogenic substrates (don’t want this because loss of protein weakens body and makes it vulnerable to infection)

47
Q

How can type 1 DM lead to ketoacidosis

A

Arises due to lack of insulin

As there’s no insulin to uptake glucose, body finds other forms of energy to use (breaking down adipose tissue to fatty acids); free fatty acids are readily used by most tissues and liver converts excess fatty acids to ketone bodies

However, if not managed with insulin injection then consistent hyperglycaemia and no insulin –> excessive ketone body production –> blood becomes too toxically acidic –> death if untreated

48
Q

How can ketones be detected clinically (2)

A

In urine and breath

49
Q

Describe how the glucose tolerance test is used to detect hyperglycaemia

A

Hyperglycaemia

Glucose tolerance test

  • fasting [BG] measured then a glucose load ingested
  • [BG] should normally return to fasting level within an hour
  • elevation of [BG] after 2 hours indicated diabetes

HOWEVER THIS TEST DOES NOT DISTINGUISH BETWEEN TYPE 1 AND 2

50
Q

How to convert plasma glucose measurement from mg/dl (US) to mM (UK)

What is 90mg/dl (=900mg/L) plasma glucose in mM/L

A

Divide the measurement in mg/dl by the molecular weight of glucose which is 180g

(900mg/L) / 180= 5mM/L

51
Q

Complications of hyperglycaemia in DM

A

Retinopathy
Neuropathy
Nephropathy
Cardiovascular Disease

Year 2 - Endocrine (21 decks)

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