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2nd year- endocrine OC > The Endocrine Pancreas 1 > Flashcards

The Endocrine Pancreas 1 Flashcards

1
Q

function of the feeding centre

A

promotes feeling of hunger and drive to eat

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2
Q

function of the satiety centre

A

promotes feelings of fullness by suppressing the feeding centres

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3
Q

what is activity in feeding centre and satiety centre controlled by?

A

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

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4
Q

what is 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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5
Q

what is 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 is a peptide hormone released by fat stores which depresses feeding activity.

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6
Q

what are the three categories of energy output?

A

cellular work- transporting molecules across membranes; growth and repair; storage of energy

mechanical work- movement, wither 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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7
Q

what are the three elements of metabolism?

A

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

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8
Q

What is an anabolic pathway?

A

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

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9
Q

what is a catabolic pathway?

A

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

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10
Q

what is 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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11
Q

when do we enter post-absorptive state?

A

Between meals and overnight the pool of nutrients in the plasma decreases

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12
Q

what is post-absorptive state?

A

where we rely on body stores to provide energy. This is a catabolic phase.

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13
Q

can the brain use fats, carbohydrates or protein for energy?

A

no they can only use glucose

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14
Q

why is it significant that the brain can only use glucose for energy?

A

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.
Failure to do so results in hypoglycaemia (low blood glucose) which can lead to coma and death.

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15
Q

what is the normal range of blood glucose concentration?

A

4.2-6.3mM

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16
Q

what is the range of hypoglycaemia?

A

<3mM

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17
Q

how does the pancreas work as an exocrine gland?

A

releasing enzymes and NaHCO3 via ducts into the alimentary canal to support digestion

99% is exocrine

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18
Q

how does the pancreas function as endocrine

A

It’s hormones are produced in the Islets of Langerhans.

only 1% is endocrine

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19
Q

what are the four types of islet cells?

A

alpha, beta, delta and F cells

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20
Q

what do alpha cells produce?

A

glucagon

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21
Q

what do beta cells produce?

A

insulin

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22
Q

what do delta cells produce?

A

somatostatin

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23
Q

what do F cells produce?

A

pancreatic polypeptide (function not really

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24
Q

what happens when glucose is taken up by cells from plasma (BG decreases)

A 
increase of:
glucose oxidation
glycogen synthesis
fat synthesis
protien synthesis
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25
Q

what happens when glucose is released into plasma from stores (BG increases)

A

increase of:
glucogenolysis
gluconeogenesis
ketogenesis

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26
Q

what stimulates glucose uptake by cells

A

insulin

27
Q

what is insulin synthesised as?

A

as a large preprohormone, preproinsulin, which is then converted to proinsulin in the ER.

28
Q

what is proinsulin packaged as? and then what happens to it?

A

packaged as granules in secretory vesicles. 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.

29
Q

what happens to insulun during the absorptive state?

A

Both glucose and aa’s stimulate insulin secretion but the major stimulus is blood glucose concentration.

Insulin dominates the absorptive state. Only hormone which lowers [BG].

30
Q

what happens to excess glucose in absorptive state?

A

stored as glycogen in liver and muscle, and as triacylglycerols (TAG) in liver and adipose tissue

31
Q

true or false:

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

A

true

32
Q

how does blood glucose concentration control insulin secretion?

A

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.

33
Q

true or false:

When [BG] is low, [ATP] is low so KATP channels are open so K+ ions flow out removing +ve charge from the cell and hyperpolarizing it, so that voltage-gated Ca2+ channels remain closed and insulin is not secreted.

A

true

34
Q

what is the only hormone that lowers blood glucose levels

A

insulin

35
Q

what is the primary action of insulin?

A

Binds to tyrosine kinase receptors on the cell membrane of insulin-sensitive tissues to increase glucose uptake by these tissues.

36
Q

do most types of tissue require insulin to take up glucose?

A

no, only muscle and dat are insulin dependent

37
Q

in other tissues, glucose uptake is via other GLUT transporters, which are not insulin dependent. What tissue uses GLUT-1?

A

Basal glucose uptake in many tissues eg brain, kidney and red blood cells

38
Q

in other tissues, glucose uptake is via other GLUT transporters, which are not insulin dependent. What tissue uses GLUT-3?

A

Basal glucose uptake in many tissues eg brain, kidney and red blood cells

39
Q

in other tissues, glucose uptake is via other GLUT transporters, which are not insulin dependent. What tissue uses GLUT-2?

A

beta-cells of pancreas and liver

40
Q

is the liver an insulin dependent tissue?

A

no

41
Q

how does the liver get glucose?

A

GLUT2 - enters down concentration gradient

42
Q

what are the additional actions of insulin

A

Increases glycogen synthesis in muscle and liver. Stimulates 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 and inhibits lipolysis.

Inhibits the enzymes of gluconeogenesis in the liver

Promotes K+ ion entry into cells by stimulating Na+/K+ ATPase. Very important clinically.***

43
Q

what are the triggers which increase insulin release?

A
  1. Increased [BG]*****
  2. Increased [amino acids]plasma
  3. Glucagon (insulin required to take up glucose created via gluconeogenesis stimulated by glucagon)
  4. Other (incretin) hormones controlling GI secretion and motility eg gastrin, secretin, CCK, GLP-1, GIP. Released by ileum and jejunem in response to nutrients. Early insulin release prevents glucose surge when absorption occurs.
  5. Vagal nerve activity (see next slide)
44
Q

what are the stimuli which inhibit insulin release?

A
  1. Low [BG]
  2. Somatostatin (GHIH)
  3. Sympathetic 2 effects
  4. Stress e.g. hypoxia
45
Q

what does vagal activity stimulate?

A

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, ie:

46
Q

what is glucagon?

A

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

47
Q

what is glucagons primary purpose?

A

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

48
Q

what are glucagon receptors?

A

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

49
Q

what are the actions of glucagon?

A

increased glycogenolysis

increased gluconeogenesis (substrates: aa’s and glycerol (lipolysis))

formation of ketones from fatty acids (lipolysis)

All these processes occur in the liver.
** Net result is elevated [BG]**

50
Q

what are the stimuli’s that promote glucagon release?

A

Low [BG] (<5mM)
High [amino acids] . Prevents hypoglycaemia following insulin release in response to aa.
sympathetic innervation and epinephrine, 2 effect
cortisol
stress e.g. exercise, infection

51
Q

what are the stimuli’s that inhibit glucagon release?

A

glucose
free fatty acids (FFA) and ketones
insulin (fails in diabetes so glucagon levels rise despite high [BG] )
somatostatin

52
Q

what is the parasympathetic innervation of islet cells?

A

increase of parasympathetic activity (vagus) leads to increase of insulin and to a lesser extent increases glucagon, in association with the anticipatory phase of digestion.

53
Q

what is the sympathetic innervation of islet cells?

A

increase of sympathetic activation promotes glucose mobilization leads to an increase of glucagon,  increase epinephrine and inhibition of insulin, all appropriate for fight or flight response.

54
Q

what is somatostatin?

A

Peptide hormone, secreted by D-cells of the pancreas

55
Q

what is the main pancreatic action of somatostatin?

A

inhibit activity in the GI Tract. Function appears to be to slow down absorption of nutrients to prevent exaggerated peaks in plasma concentrations. (Synthetic SS may be used clinically to help patients with life-threatening diarrhoea associated with gut or pancreatic tumours).

56
Q

is somatostatin a counter-regulatory hormone in the control of blood glucose?

A

no but it does strongly suppresses the release of both insulin and glucagon in a paracrine fashion.

57
Q

what is the effects of exercise on blood glucose concentration

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 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

what happens in starvation?

A

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

59
Q

what is type 1 diabetes?

A

Autoimmune destruction of the pancreatic -cells destroys ability to produce insulin and seriously compromises patients ability to absorb glucose from the plasma. 10% of diabetic patients are insulin-dependent.

60
Q

what is type 2 diabetes?

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.

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

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

61
Q

what are the diabetes type 2 treatment?

A

Initial treatment is aimed at trying to restore insulin sensitivity of tissues with exercise and dietary change

If this fails, oral hypoglycaemic drugs will be used, Metformin is the first line treatment

Sulphonylureas are a class of drug which act to close the KATP in  cells and stimulate Ca2+ entry and insulin secretion. 
Obviously requires functioning  cells, so cannot be used to treat type I.
62
Q

why is [BG] elevated in both type 1 and type 2?

A

type 1-inadequate insulin release

type 2- inadequare tissue response

63
Q

why is hyperglycaemia bad?

A

glucose is a highly reactive molecule which can eventually produce long-term problems that may be very serious

leads to
retinopathy
neuropathy
nephropathy
cardiovascular disease
64
Q

why is hypoglycaemia bad?

A

leads to coma and brain death

2nd year- endocrine OC (27 decks)

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