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Endocrinology & Reproduction > Growth hormone > Flashcards

Growth hormone Flashcards

1
Q

what is growth hormone

A

a single chain polypeptide

191 amino acids 22kDa Inhumans

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2
Q

what hormones does growth hormone have high structural homology with

A

PL and PRL

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3
Q

is GH universal across species

A

no - highly specifies specific. Must use hGH for treating human deficiencies

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4
Q

how does GH circulate

A

in plasma bound to GH binding protein

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5
Q

half-life of GH

A

~50 minutes = relatively long

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6
Q

when do levels of GH rise

A

puberty

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7
Q

when does GH peak

A

adulthood/maturity

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8
Q

where is GH synthesised

A

anterior pituitary

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9
Q

where is GH secreted

A

anterior pituiatry

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10
Q

what stimulates GH secretion

A

GHRH and ghrelin

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11
Q

what inhibit GH secretion

A

somatostatin

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12
Q

when does maximum GH secretion occur

A

during sleep

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13
Q

gender differences of GH

A

women secrete ~3 times more GH per day

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14
Q

GH receptor

A

cytokine family

widely expressed in most cells

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15
Q

what happens when GH binds to GHR

A

causes the GHR to dimerise and activates the JAK2/STAT signalling cascade

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16
Q

GHR knockout mice

A

no expression of GHR
Severe post natal growth retardation
no change at birth weight
still some growth, probs through insulin

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17
Q

what kind of growth retardation occurs in knockout GHR mice

A

proportionate dwarfism and delayed puberty

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18
Q

how does growth occur in GHR knockout mice

A

probably insulin signalling

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19
Q

GH has a direct effect on growth

A

FALSE

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20
Q

GH has an indirect effect on growth

A

TRUE

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21
Q

how does GH stimulate growth

A

via secretion of IGF-1

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22
Q

IGF-1

A

insulin like growth factor

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23
Q

what stimulates secretion of IGF-1

A

GH

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24
Q

what does IGF-1 stimulate

A

growth

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25
Q

where is IGF-1 secreted

A

liver

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26
Q

what triggers secretion of IGF-1 from the liver

A

GH binding to GHR

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27
Q

how des IGF-1 travel

A

in plasma bound to proteins, there are at least 6 different IGF-1 binding proteins

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28
Q

half life of IGF-1

A

10 minutes

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29
Q

how is half life of IGF-1 increased

A

binding it IGF-1 binding proteins, increases to 3 hours

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30
Q

when does IGF-1 have half life of 3 hours

A

when bound to IGF1 binding proteins

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31
Q

how does IGF-1 work

A
  • binds to the cell surface of IGF-1 receptors
  • increases protein synthesis
  • cartilage formation and bone growth
  • increases growth of all organs
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32
Q

GHRH

A

growth hormone releasing hormone

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33
Q

where is GHRH released

A

ARC nucleus in the hypothalmus

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34
Q

where is the ARC nucleus

A

hypothalamus

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35
Q

where does GHRH go

A

released from ARC

travels in portal system to anterior pituitary somatotropin to stimulate GH

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36
Q

What does GHRH stimulate

A

GH

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37
Q

what has a similar effect to GHRH

A

ghrelin

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38
Q

what happens in the JAK/STAT cascade

A

STAT dimers drive the IGF-1 gene transcription and translation

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39
Q

what drives the transcription and translation of IGF-1

A

JAK/STAT signallig cascade

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40
Q

what happens when IGF-1 reaches receptor cells e.g bone

A

undergoes signal transduction cascades through receptor activation = growth

41
Q

what is the negative feedback of GH

A

IGF-1 released from the liver binds to receptors on anterior pituitary somatotropin which inhibits GH secretion

42
Q

how does bone growth occur

A

activation of cartilage growth plates located between shaft and head

43
Q

proper name of growth plates

A

epiphyseal plates

44
Q

where are epiphyseal plates located

A

between the shaft and the head

45
Q

how does IGF-1 effect bone growth

A

induces formation of new cells that cause the shaft to increase in length at both ends

46
Q

when is ossification complete

A

~25 years old

47
Q

how do we know IGF-1 mediates growth promoting effects of GH

A

mice
IGF-1 knockout = severe growth retardation
wt and knockout same weight at birth
similar traits to GHR knockout. Both have no IGF-1

48
Q

What kind of receptor is IGF-1 receptor

A

tyrosine kinase

4 subunits; 2 alpha outside cell, 2 beta transmembrane

49
Q

what receptor is IGF1R similar to

A

insulin receptor

50
Q

where does IGF-1 bind to IGF1R

A

extracellular domain - alpha

51
Q

how are the alpha and beta subunits of IGF1 R bound to eachother

A

disulphide bonds // cystein residues

52
Q

what does it mean that the IGF1 R is kinase

A

it has enzyme activity

53
Q

what is the enzyme activity of the IGF1 R

A

when IGF1 binds, induces a conformational change
tyrosine kinase within beta subunits becomes activated
autophosphorylation of the intracellular residues
= signalling inside the cell

54
Q

how does IGF1R work

A

when IGF1 binds to extracellular alpha domain, induces a conformational change
tyrosine kinase within beta subunits becomes activated
autophosphorylation of the intracellular residues
= signalling inside the cell

55
Q

intracellular signalling of IGF1-R

A

MAPK is coupled to mitogenesis
PKB pathway results in protection against apoptosis
= net effect of growth promotion

56
Q

how does intracellular signalling of IGF1-R result sin growth promotion

A

MAPK is coupled to mitogenesis and PKB protects against apoptosis

57
Q

what does MAPK do fro growth

A

coupled to mitogenesis

58
Q

what does PKB do for growth

A

protects against apoptosis

59
Q

what causes proportionate dwarfism

A

deficiency in GH

60
Q

reduced cell growth can arise from

A
  • decreased GH secretion
  • defects in GH receptor
  • defects in IGF-1 secretion
  • defects in IGF-1 receptor
61
Q

causes of decreased GH secretion

A
  • GHRH receptor gene mutations
  • anterior pituiatry failure
  • GH gene mutations
62
Q

what causes isolated GH deficiency

A

GHRH receptor gene mutations

63
Q

how to treat decreased GH secretins

A

GH injections

64
Q

what else is affected if GH is decreased from anterior pituiatry failure

A

TSH leading to metabolic defects

65
Q

what causes defects in GH receptor

A

mutated GHR, GH resistance

66
Q

example of GH receptor defects

A

Laron syndrome

67
Q

laron syndrome

A

GH receptor defect

68
Q

Plasma levels of GH and IGF1 in Laron syndrom

A

IGF-1 - low because GH cant stimulate secretio

GH- high because no IGF-1 for negative feedback

69
Q

treatment of defects in GH receptor

A

IGF-1 injections

70
Q

what causes defects in IGF1 secretion

A

IGF-1 gene deletion

71
Q

Plasma levels of GH and IGF1 when defects in IGF1 secretion

A

IGF1 levels undectable in plasma

GH - high because no IGF-1 for negative feedback

72
Q

treatment of defects in IGF-1 secretion

A

IGF-1 injections

73
Q

what requires treatment of GH injections

A

decreased GH secretion

74
Q

what requies treatment of IGF1 injections

A

impaired GH receptor, defects in IGF1 secretion

75
Q

how to treat defects in IGF1 receptor

A

can’t - its embryonically lethal becuase IGF1R plays key role in development of embryo

76
Q

which growth defect is embryonically lethal

A

defects of the IGF1 receptor

77
Q

when must treatments of GH or IGF1 problems be done

A

before end of puberty becuase that’s when bones fuse

78
Q

why must GH and IGF1 treatments be done before end of puberty

A

bones fuse

79
Q

excess GH causes

A

gigantism

80
Q

when is GH over secreted to cause gigantism

A

pre puberty

81
Q

gigantism

A

over secretion of GH pre puberty

82
Q

what does excess GH in childhood commonly cause

A

benign pituitary adenoma

83
Q

what does excess GH in childhood raraely cause

A

gigantism

84
Q

is gigantism proprtionate

A

yes; excess GH is pre puberty and so growth plates havent fused so there excessive height in proportionate with growth

85
Q

treatment for gigantism

A

somatostatin analogues

86
Q

treatment of most common effect of excess GH prepuberty

A

removal of benign pituitary adenoma

87
Q

over secretion of GH post puberty causes

A

acromegaly

88
Q

acromegaly

A

over secretion of GH post puberty

89
Q

characteristics of acromegaly

A

thickiening of bones in the jaw, fingers and toes

90
Q

why is acromegaly different to gigantism

A

growth plates have fused post-puberty, giving different effects in acromegaly

91
Q

what does GH effect directly

A

metabolism

92
Q

what does GH effect indirectly

A

growth

93
Q

how does GH relate to inuslin

A

GH is counter-regualtory hormone that antagonises the effects of insulin

94
Q

does GH antagonise or agonise the effects insulin

A

antagonise

95
Q

when is GH present metabolically

A

fasting

96
Q

effects of GH in fasting

A
  • increases lipolysis

- increases gluconeogenesis

97
Q

what do the metabolic effects of GH prevent

A

they prevent hypoglycaemia when fuels are low by maintaining the balance of blood glucose
- lipolysis and gluconeogenesis

98
Q

how does GH oppose the effects of insulin

A

Growth hormone makes muscle and adipose tissue less responsive to insulin (‘insulin resistant’) and so reduces glucose uptake by these tissues which reduces the storage of glucose during the absorptive phase and maintains high circulating levels of glucose. In this way growth hormone opposes the metabolic effects of insulin.

Endocrinology & Reproduction (15 decks)

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