The endocrine pancreas Flashcards

1
Q

what is the difference between anabolic and catabolic pathways?

A

anabolic pathways build up and store energy for when required
catabolic pathways breakdown and release energy required for work

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2
Q

what is the name of the process by which glucose is synthesised from glycogen?

A

glycogenolysis

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3
Q

what is the name of the process by which glucose is synthesised from amino acids?

A

gluconeogenesis

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4
Q

what is the normal range of blood glucose?

A

4.2 - 6.3mM

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5
Q

what is the blood glucose level of someone hypoglycaemic?

A

< 3mM

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6
Q

what hormones does each f the 4 pancreatic cells produce?

A

A cells = glucagon
B cells = insulin
delta cells = somatostatin
F cells = pancreatic polypeptide

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7
Q

when proinsulin is cleaved it gives insulin and what other molecule?

A

C-peptide

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8
Q

what is the main stimulus of insulin secretion?

A

glucose

AA’s also stimulate insulin release but glucose is the main one

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9
Q

how does an increase in glucose cause insulin secretion?

A

when glucose levels rise, it enters the cell via GLUT transporters
this increases ATP within the cell which causes the Katp channel to close
closing the K channel = rise in K in the cell causing depolarisation
depolarisation triggers opening of voltage gated Ca channels
influx of Ca triggers insulin vesicles exocytosis into the circulation

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10
Q

what type of glucose transporter is insulin dependant and where is this found?

A

GLUT 4 in muscle and fat tissue

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11
Q

where is GLUT 1, GLUT 2 and GLUT 3 transporters found?

A

GLUT 1 & 3 = many tissues i.e. brain, kidney, RBC’s

GLUT 2 = B cells of pancreas and liver

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12
Q

via what transporter does glucose enter the liver and why is this significant?

A

GLUT 2
glucose enters the liver independent of insulin status
glucose moves down a concentration gradient into the liver
(however insulin is required for transport into hepatocytes)

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13
Q

what enzyme does insulin trigger which lowers blood glucose concentration?

A

hexokinase

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14
Q

what hormone inhibits insulin release and how?

A

somatostatin (GHIH)
somatostatin decreases GI motility therefore release of glucose into blood stream and so glucose levels aren’t detected as quick

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15
Q

why is the release of insulin in response to glucose via oral administration greater the that of IV administration?

A

with oral administration, vagal activity also stimulates the release of other GI hormones which stimulate insulin secretion

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16
Q

what hormones form the glucose counter-regulatory control system?

A

glucagon
epinephrine
cortisol
growth hormone

17
Q

what type of receptors are glucagon receptors?

A

G-rpotein coupled receptors

18
Q

what is the actions of glucagon?

A

glucagon phosphorylates;
increase glyconeolysis
increase gluconeogenesis
formation of ketones from free fatty acids

19
Q

after a high protein meal with little carbohydrate, how does our blood glucose maintain within normal range?

A

amino acids trigger the release of both insulin and glucagon

because since amino acids trigger the release of insulin, since the meal has little sugar this would result in hypoglycaemia. but since it also stimulates glucagon, it can trigger gluconeogenesis

20
Q

does somatostatin inhibit or promote glucagon release?

A

inhibit

21
Q

does vagal activity increase or decrease insulin release?

A

increase

22
Q

during exercise, how does glucose entry into skeletal muscle increase?

A

entry into the skeletal muscle during exercise is insulin independent
GLUT 4 transporters migrate (even though in non exercising tissue they are insulin dependant)

23
Q

what is used as an energy source in order to spare the breakdown of protein?

A

conversion of free fatty acids to ketones

24
Q

how does type 1 diabetes result in ketoacidosis?

A

they are unable to produce insulin
the uptake of glucose is insulin dependant, therefore glucagon causes gluconeogenesis converting FFA’s into ketones
this is because there is low glucose concentration within the cell
(the body thinks it has low glucose, but it is actually really high in the plasma)
ketone absorption is also insulin dependant therefore there is a build up of ketones within the plasma resulting in acidosis