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Endocrinology > Insulin Secretion & Signalling > Flashcards

Insulin Secretion & Signalling Flashcards

1
Q

which cells in the body make insulin?

A

beta cells in the pancreas

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2
Q

how is insulin secreted from beta cells?

A

directly into the blood

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3
Q

what do alpha cells secrete?

A

glucagon

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4
Q

what do delta cells secrete?

A

somatostatin

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5
Q

what do PP cells secrete?

A

pancreatic polypeptide

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6
Q

what is the preprohormone of insulin called?

A

preproinsulin

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7
Q

where is preproinsulin formed?

A

in the RER of pancreatice beta cells

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8
Q

what does insulin look like?

A

two polypeptide chains linked by disulfide bonds

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9
Q

what happens to preproinsulin to make insulin?

A

it’s cleaved

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10
Q

is animal or human insulin preferred and why?

A

animal insulin creates a slight antigenic reaction in the body when given for long periods of time so human insulin is preferred

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11
Q

how does glucose enter beta cells from the blood?

A

through GLUT2 glucose transporter

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12
Q

what phosphorylases glucose in beta cells & wheat does this produce?

A

glucose -> glucose-6-phosphate

by glucokinase

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13
Q

is glucokinase’s Km for glucose within or out with the physiological range of glucose?

A

within

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14
Q

what does having a Km within the physiological range of glucose mean glucokinase can do?

A

phosphorylate glucose quickly in reaction to a small change, maintain normal range

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15
Q

does the metabolism of glucose need to increase or decrease to increase intracellular ATP concentration?

A

increase

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16
Q

how many ATP are produced in the metabolism of one glucose molecule?

A

36

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17
Q

what does ATP do in the secretion of insulin?

A

inhibits ATP-sensitive K+ channel Katp

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18
Q

what does the inhibition of Katp lead to in the secretion of insulin?

A

depolarisation of the cell membrane

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19
Q

what does the depolarisation of the cell membrane cause in the secretion of insulin?

A

opening of voltage-gated Ca2+ channels

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20
Q

what does an increase in internal Ca2+ concentration lead to in the secretion of insulin?

A

fusion of secretory vesicles with the cell membrane& release of insulin

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21
Q

how many phases are there in the release of insulin?

A

2

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22
Q

what is the 1st phase of insulin release in response to?

A

immediately after a large bolus of glucose entering the body to prevent a rapid rise in blood glucose

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23
Q

what is the purpose of the 2nd phase of insulin release?

A

to maintain the correct levels of glucose in the blood

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24
Q

which two proteins make up the Katp channel?

A

Kir6.1

SUR1

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25
Q

what is Kir6.1 & what does it do?

A

an inward rectifier subunit

pore subunit

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26
Q

what is SUR1 & what does it do?

A

sulphoylurea receptor

regulatory subunit

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27
Q

what does the Katp channel exist as?

A

an octomeric structure

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28
Q

which class of drug directly inhibits the Katp channel?

A

sulphonylurea

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29
Q

which drug stimulates Katp to inhibit insulin secretion?

A

diazoxide

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30
Q

if a patient is produces too much insulin what do you want to do to the Katp channel & which drug would use?

A

stimulate the Katp channel

use diazoxide

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31
Q

if a patient is producing too little insulin what do you want to do to the Katp channel & which drugs would you use?

A

inhibit the Katp channel

sulphonylurea

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32
Q

in humans what can mutations of Kir6.1 mutations cause?

A

neonatal diabetes

- activated Katp channels or increase in Katp numbers

33
Q

what can some Kir6.1 or SUR1 mutations lead to?

A

congenital hyperinsulinism

- trafficking/inhibiting mutations

34
Q

what does MODY stand for?

A

maturity-onset diabetes of the young

35
Q

what is MODY?

A

a familial form of early-onset type 2 diabetes

36
Q

what causes MODY?

A

genetic defect in beta cell function cause monogenic diabetes

37
Q

what happens to insulin secretion in MODY?

A

primary defects in insulin secretion (don’t secrete properly)

38
Q

mutations in what can cause MODY?

A

6 different mutations:

  • 1 for glucokinase
  • 5 for transcription factors
39
Q

which 2 ways can MODY be caused?

A
  • glucokinase activity is impaired

- glucose sensing defect, threshold for insulin secretion is increased

40
Q

how would a patient with MODY present?

A

like a type 1 diabetes patient but older

41
Q

what do HNF transcription factors do?

A
  • play key role in pancreas foetal development & neogenesis
  • regulate beta cell differentiation & function
42
Q

what’s the difference in treatment of type 1 diabetes & MODY?

A

type 1 diabetes - insulin

MODY - sulphonylurea

43
Q

what happens in type 1 diabetes?

A

loos of insulin secreting beta cells

44
Q

what happens in type 2 diabetes?

A

initially hyperglycaemia with hyperinsulinaemia so insulins sensitivity in tissues is reduced

45
Q

to which family of receptors does insulin’s receptor belong to?

A

receptor tyrosine kinases

46
Q

what do kinases do?

A

promote phosphorylation

47
Q

what is phosphorylation?

A

addition of a phosphate group

48
Q

which enzymes reverse phosphorylation?

A

phosphatases

49
Q

which chemical group is the phosphate acceptor on a protein molecule?

A

the hydroxyl group

50
Q

what does a phosphate group do to the charge of a protein structure?

A

introduces a large negative charge

51
Q

what is the insulin receptor structure like?

A

dimeric

52
Q

what is the insulin receptor made of?

A

2 extracellular alpha subunits

2 transmembrane beta subunits

53
Q

what do the 2 alpha subunits of the insulin receptor have?

A

insulin binding domains

54
Q

what are the subunits of the insulin receptor linked by?

A

disulfide bonds

55
Q

what do the beta subunits have the ability to do?

A

bing ATP

56
Q

what does binding of insulin do to the alpha subunits do?

A

causes beta subunits to phosphorylate themselves

57
Q

what does the autophosphorylation of the beta subunits of the insulin receptor do?

A

activates the catalytic activity of the insulin receptor to all the substrates to be phosphorylated

58
Q

what does IRS (substrate of insulin receptor) activating the RAS pathway do?

A

activates MAP kinase pathway & gene expression

59
Q

what does IRS activating PI3K do?

A

activates PKB which causes glycogen synthesis

60
Q

what does PKB stimulate?

A

GLUT4 translocation into the cell

61
Q

what serious side effect can arise from the over stimulation of insulin signalling?

A

cancerous issues can arise

62
Q

name some of the biological effects of insulin

A
  • amino acid uptake in muscle
  • DNA synthesis
  • protein synthesis
  • growth responses
  • glucose uptake in muscle & adipose tissue
  • lipogenesis in adipose tisse & liver
  • glycogen synthesis in liver & muscle
  • gene expression
  • lipolysis & gluconeogenesis in liver
63
Q

what is the inheritance pattern of leprechaunism?

A

rare autosomal recessive

64
Q

where does the mutation occur in leprechaunism?

A

mutations in gene for insulin receptor

65
Q

what happens in leprechaunish?

A

severe insulin resistance due to defects in insulin binding or insulin receptor signalling

66
Q

what are the abnormalities found in leprechaunism?

A
  • elfin facial appearance
  • growth retardation
  • absence of subcutaneous fat, decreased muscle mass
67
Q

what is the other name for leprechaunish?

A

donohue syndrome

68
Q

what is the inheritance pattern of Rabson Mendenhall Syndrome?

A

rare autosomal recessive

69
Q

what happens in raisin mendenhall syndrome?

A

severe insulin resistance, hyperglycaemia & compensatory hyperinsulinaemia

70
Q

what are the characteristics of raisin mendenhall syndrome?

A
  • developmental abnormalities
  • acanthosis nigricans (hyperpigmentation)
  • fasting hypoglycaemia
  • DKA
71
Q

where are ketone bodies formed?

A

in liver mitochondria

72
Q

what are ketone bodies derived from?

A

acetyl-coa from beta oxidation

73
Q

how do ketone bodies leave the liver?

A

diffuse into the blood stream & move to peripheral tissues

74
Q

what are ketones important for?

A

molecules of energy metabolism for heart muscle & renal cortex

75
Q

what reaction does acetyl-CoA come from?

A

fatty acid oxidation

76
Q

what can the accumulation of ketone bodies lead to?

A

acidosis

77
Q

what is the most common clinical symptoms of DKA?

A

dehydration (exacerbates acidosis)

78
Q

name 3 important ketone bodies

A
  • acetone
  • acetoacetic acid
  • beta-hydroxybutyric acid
79
Q

which type of diabetes is most associated with DKA?

A

type 1 when insulin has not been injected, cells fail to receive enough glucose & switch to fat breakdown

Endocrinology (23 decks)

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