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Endocrine > Pancreas > Flashcards

Pancreas Flashcards

1
Q

what does the feeding centre promote?

A

feelings of hunger and a drive to eat

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2
Q

what does the satiety centre promote?

A

feelings of fullness (by suppressing the feeding centre)

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3
Q

describe the glycostatic theory controlling the energy intake

A

food intake is determined by the blood glucose. as it increases the drive to eat decreases.

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4
Q

describe the lipostatic theory controlling energy intake

A

food intake is determined by fat stores. as fat stores increase the drive to eat decreases.

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5
Q

what is leptin?

A

a peptide hormone released by fat stores to depress feeding centres

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6
Q

what are the three categories of energy output?

A

> cellular work
mechanical growth
heat loss

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7
Q

what is metabolism?

A

integration of all biochemical reactions in the body

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8
Q

what is the net effect in anabolic pathways?

A

synthesis of large molecules from smaller ones usually for storage purposes

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9
Q

what is the absorptive state?

A

the state we enter after eating a meal where digested nutrients supply the energy needs of the body and excess is stored

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10
Q

what is the net effect in catabolic pathways?

A

there is breakdown of large molecules into smaller ones, releasing energy for work

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11
Q

what is the post-absorptive state?

A

where we really on body stores to provide energy as the nutrients in the plasma decrease.

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12
Q

what is glycogenolysis?

A

making glucose from glycogen

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13
Q

what is gluconeogenesis?

A

making glucose from amino acids

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14
Q

what is glycogenesis?

A

making glycogen from glucose

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15
Q

what is the normal range for glucose?

A

4.2-6.3mM

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16
Q

name the 4 cell types in the islets of Langerhans

A

> alpha cells
beta cells
delta cells
F cells

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17
Q

what do alpha cells produce?

A

glucagon

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18
Q

what do beta cells produce?

A

insulin

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19
Q

what do delta cells produce?

A

somatostatin

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20
Q

what do f cells produce?

A

pancreatic polypeptide (help nutrient absorption from GI)

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21
Q

where is preproinsulin converted to proinsulin?

A

in the rough endoplasmic reticulum in beta cells

22
Q

what is proinsulin split into?

A

> insulin

> c peptide

23
Q

what is the effect of insulin on excess glucose stored?

A

> as glycogen in the liver and muscles

> as triacylglycerols in the liver and adipose

24
Q

what is the effect of insulin secretion on amino acids?

A

they are made into new proteins and the excess is converted to fat

25
Q

what is the effect of insulin secretion on fatty acids?

A

they are stored in the form of triglycerides in the adipose tissue and liver

26
Q

what triggers insulin secretion?

A

high glucose levels in the blood

27
Q

how is metabolism affected by insulin?

A

it is increased

28
Q

describe how glucose causes insulin secretion

A

> glucose enters the cell through a GLUT transporter
it increases cellular ATP
this ATP causes the cell to depolarise
this opens Ca2+ channels which acts as an intracellular signal
this triggers exocytosis and secretion of insulin

29
Q

describe the action of insulin on a cell

A

> insulin binds to a tyrosine kinase receptor
signal transduction cascade mobilises GLUT4 which migrates to the membrane
glucose is transported into the cell

30
Q

what happens to GLUT4 transporters when insulin stimulation stops?

A

they return to the cytoplasmic pool

31
Q

what receptor does insulin bind to?

A

tyrosine kinase receptor

32
Q

what cells are sensitive to insulin?

A

muscle and fat cells

33
Q

what transporters are involved in non-insulin dependent glucose uptake?

A

GLUT 1, 3 and 2

34
Q

what are glut 1 and 3 transporters used for?

A

basal glucose uptake in tissues like the brain, kidney and RBC

35
Q

what cells take up glucose via GLUT 2?

A

> beta cells of the pancreas

> liver cells

36
Q

how does insulin indirectly alter glucose transport?

A

insulin activates hexokinase which lowers intracellular glucose concentration creating a gradient that moves glucose into cells.

37
Q

what hormone is insulin permissive to?

A

growth hormone

38
Q

what is the effect of insulin of potassium ion entry to the cell?

A

insulin stimulates Na/K ATPase allowing potassium to enter the cell.

39
Q

what stimulates insulin release?

A 
> vagal nerve activity
> increased amino acids
> increased blood glucose concentration
> glucagon
> incretin hormones controlling GI secretion and motility
40
Q

what inhibits insulin release?

A

> low [BG]
somatostatin
sympathetic alpha2 effects
stress (hypoxia)

41
Q

is IV glucose load more or less than the equivalent amount of glucose given orally?

A

it is less:

oral glucose increases insulin by direct effect on beta cells AND vagal stimulation of beta cells AND incretin effects

42
Q

what are the effects of glucagon?

A

increased:
> gycogenolysis
> gluconeogenesis
> ketogenesis

43
Q

what cells produce glucagon?

A

alpha cells

44
Q

at what blood glucose level will secretion of glucagon increase dramatically?

A

<5.6mM

45
Q

what stimulates glucagon secretion?

A 
> stress
> cortisol
> low [BG]
> high [amino acid]
> sympathetic innervation (epinephrine)
46
Q

what inhibits glucagon release?

A 
> glucose
> free fatty acids
> ketones
> insulin
> somatostatin
47
Q

what cells in the pancreas produce somatostatin?

A

D cells

48
Q

what is the main pancreatic function of somatostatin?

A

inhibition of activity in the GI tract: slowing down absorption of nutrients to prevent exaggerated peaks in plasma concentration

49
Q

what is the effect of somatostatin on insulin and glucagon?

A

it supresses the release of these hormones in a paracrine fashion

50
Q

what is the effect of exercise on insulin sensitivity?

A

it increases sensitivity

51
Q

true or false:

in type 2 diabetes there can be hyperinsulineamia

A

true: beta cells ca remain intact so will continue to produce lots of insulin to try and over come the desensitisation of peripheral tissues

52
Q

does a glucose tolerance test distinguish between type 1 an 2 diabetes?

A

no it doesn’t

Endocrine (15 decks)

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