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kris Endocrinology > 5 > Flashcards

5 Flashcards

1
Q

Do cells only make one type of hormone?

A

No

Hormones are co-expressed, meaning that one cell produces more than one hormone

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2
Q

Are there cells that produce TSH only

A

no
there is no cells that will produce just TSH ( thyroid stimulating hormone) beta, thus TSH comes from cells that produce other hormones as well

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3
Q

Are there cells that produce GH only?

A

60-70% GH+ cells express only GH and no other hormones

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4
Q

Are there cells that produce PRL only?

A

6-16% PRL+ cells express only PRL

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5
Q

WHat is the sexual dimorphism factor of PRL?

A

Cells that produce PRL only are more found more frequently in females than males

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6
Q

Are two types of gonadotrophs produced by 2 different cells?

A

Gonadotropin producing cells produce both LH and FSH, no singularity-> Both gonadotrophs are co-expressed

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7
Q

What is a somatotroph?

A

Somatortropin (GH) producign cells

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8
Q

How is GH stored?

A

in granules in the cytoplasm of somatotrophs

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9
Q

WHat is the most abundant type of endocrine cell in the anterior pituitary?

A

somatotroph

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10
Q

Pituitary contains about __-__ mg of GH

A

Pituitary contains about 5-15 mg of GH

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11
Q

WHat is the release of GH dependent on

A

on it’s release from storage granules, not on it’s levels of production necessarily

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12
Q

What are the types of GH genes? Where are they found?

A

The five-member human growth hormone (hGH)/chorionic somatomammotropin (hCS) gene cluster encodes the pituitary-specific hGH-N gene expressed in pituitary somatotropes, and four highly related genes (hGH-V, hCS-A, hCS-B, and hCS-L) that are expressed only in the placenta.

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13
Q

What is so special about the hCS-V isoform?

A
  • non-functional/non-expressed in males
  • hCS-V increases midgestation
    It is expressed in placenta-> after delivery (no placenta)-> hCS-V disappears from circulation within hours
    has an affect on the mother- when levels go up in the gestation- GH levels go down in the mother - after mid-gestation GH levels go don in the mother
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14
Q

How are hGH genes regulated? How are they dipsered in the genome

A

these are controlled by upstream sequences

these genes are presnet in one region of human genome

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15
Q

What are the 2 forms of GH gene? How do they differ

A
  • Major form 22 kDa (191 a.a);
    Shorter isform (20 kD) with aa 32-46 missing, contributes 10% of GH pool
  • these are the same gene- shorter isoform is produced by post-translational splicing
    -There are subtle differences in the spectrum of bioactivities + degree of glycosylation
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16
Q

What can Human GH be used for?

A

for treatment of pituitary dwarfism

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17
Q

What is the problem with cadaver-sourced GH

A

prion contamination

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18
Q

GH is secreted by the __ pituitary gland in a __

A

GH is secreted by the anterior pituitary gland in a pulsatile manner under the acute stimulatory effects of the hypothalamic peptide GH-releasing hormone (GHRH) and the inhibitory effects of somatostatin.

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19
Q

What are the 2 main factors that control GH release (stimulatory and inhibitory)
What is the source of these factors

A

Hypothalamus releases these factors
stimulatory- hypothalamic peptide GH-releasing hormone (GHRH)
inhibitory - somatostatin

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20
Q

__ and __ neurons integrate stimulatory and inhibitory inputs to regulate pituitary GH secretion

A

GHRH and Somatostatin neurons integrate stimulatory and inhibitory inputs to regulate pituitary GH secretion

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21
Q

What are some of stimulatory factors that act on GHRH? and thus the release of GH

A

deep sleep
fasting
hypoglycaemia
gherlin

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22
Q

What are some of suppressing factors that act on SRIF? and thus the inhibtion release of GH

A 
obesity
glucose
hypothyroidism 
IGF-1
FFA
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23
Q

What is a treatment that induces GH secretion? How does it affect various sexes

A

GHRH treatment induces GH secretion (♀response > ♂)

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24
Q

Which hormone inhibits GH secretion

A

somatostatin

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25
Q

When is 2/3rd of GH released

A

in slow-wave sleep/deep sleep

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26
Q

What are the GH levels throughout the life stages?

A

Levels fetus (highest) > child < adolescent (big increase in GH levels) > adult

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27
Q

What is the potency of the effect of GH depended on?

A

Changes in amplitude (the amount released) but not frequency of pulses

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28
Q

What is the hypothalamus-pituitary-liver axes?

A

Hypothalamus-> GHRH-> GH production from pituitary-> GH stimulates the production of IGF-1 in the liver

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29
Q

WHat is the master regulator of GH release

A

hypothalamus

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30
Q

How is GH found in the circulation?

A

GH is found in circulation in bound to a protein

GH is bound to GHBP – extracellular domain of GHR This also regulates the half-life of GH

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31
Q

How does GH bind to a receptor and phosphorylates it? What happens after phosphorylation

A

GH is a tyrosine kinase receptor signal that uses adaptor protein-> GH receptor has no auto-phosphorylation capacity-> needs an adaptor
GH receptor uses JAK2
-> JAK2 self-phosphorylates and phosphorylates the receptors

32
Q

In which form are the ligands who’s receptor needs an adaptor protein found?

A

Ligands that require an adaptor protein are found in pre-dimerized form, before they bind to a protein and after binding to the receptor, they cannot autophosphorylate -> have to recruit a tyrosine kinase

33
Q

Which pathways/outcomes can JAK2 lead to?

A

GH+JAK2-> MAPK-> cell proliferation
GH+JAK2-> PI3K-> glucose metabolism
GH+JAK2-> STAT-> IGF-1

34
Q

What is the effect of STAT pathway?

A

STAT is a transcription factors, has multiple target genes including suppressors of cytokine signalling (SOCS)
SOCS are inhibitors of STAT signal - stat signal is this case comes from GH
SOCS thus inhibit GH signalling
SOCS also result in IGF-1 formation which has an inhibitory effect on GH release

35
Q

What happens to SOCS-2 knockout mice? Why?

A

They were gigantic

suppressor of cytokine signalling (SOCS) inhibits GHR signalling

36
Q

What is the direct action of GH

A

Promotion of cell

differentiation

37
Q

What is the indirect action of GH

A

Induction of IGF-I production by liver cells that can act as proliferative and differentiating gene;
also stimulates other proteins that are necessary for this IGF-1 pathway - IGFBP-3 (IGF binding protein) and ALS

38
Q

How does IGF-1 found in the circulation?

A

as a bound protein

39
Q

What is the role of proteases in IGF-1 pathway

A

proteases free IGF-1 from IGF binding protein

They are also stimulated by GH

40
Q

WHat is the function of IGF-1

A

proliferation and differentiation of cells

41
Q

Where is IGF-1 produced?

A

mainly in the liver but is also produced locally under the influence of GH (regulation of local growth)

42
Q

How does GH promotes growth

A

GH induces growth directly by acting on cells through GH receptors, but most of it comes inderectly from stimulating IGF-1 system

43
Q

When is IGF-1 growth system important

A

in childhood

44
Q

IGF-I levels __ growth rate in children

A

IGF-I levels parallel growth rate in children

45
Q

What is the effect of GH and IGF-1 on bones

A

GH and IGF-I promote growth of long bones at the epiphyseal plates (proliferation (differentiate through calcification) of cartilage cells, i.e. chondrocytes).

46
Q

When does bone growth finish?

A

Epiphyses fuse at the end of puberty and longitudinal growth ceases

47
Q

Does auricular cartillage calcify?

A

no- it’s a cushioning for bone interaction

48
Q

GH metabolic effect in adults

A

optimizes body composition, physical function and substrate metabolism
- regulated partially by GH, but GH influences effects of other genes to regulate these processes
Interacts with insulin to regulate Glu, fat and protein metabolism

49
Q

GH effect on fat

A

Enhances lipolysis and FA oxidation – improved during fasting (fatty oxidation of energy is stimulated in muscles
allows for use of non-glucose nutrients- useful in fasting)

50
Q

GH effect which is beneficial in fasting

A
  • Enhances lipolysis and FA oxidation – improved during fasting (fatty oxidation of energy is stimulated in muscles-> allows for use of non-glucose nutrients- useful in fasting)
  • Reduces urea synthesis and excretion – Protein sparing
51
Q

GH effect on glucose uptake

A
  • Inhibits insulin stimulated glucose uptake

- Also, GH treatment induces insulin secretion and glucose uptake

52
Q

GH effect on AA uptake and protein synthesis

A

Increases AA uptake and protein synthesis

53
Q

Describe IGF-I

A

IGF-I: GH-dependent

  • Produced by the liver and other tissues. IGF-I from the liver is released into the blood stream.
  • Other tissues - local production and paracrine/autocrine.
54
Q

Describe IGF-II

A 
IGF-II: GH-independent
- Important in fetal development. 
Role in adults less clear. May
act via IGF-I receptors.
May not be important beyond fetal development
55
Q

Describe IGF-binding proteins

A
  • Secreted by target cells together with specific proteases.
  • May regulate bioavailability and turn-over of IGFs
56
Q

Structure of IGFs is similar to _

A

Structure of IGFs is similar to insulin

57
Q

What dictates the bioavailability of IGF-1?

A

IGF-binding proteins allow tissued to regulate local IGF-I signalling
IGF-I is an endocrine hormone that has a set of binding proteins that bind and hold IGF-I-> not bioavailable
Binding protein proteases can be released by tissues -> affects how much IGF-I is bioavailable
thus levels of IGF-1 released by the liver does not necessarily dictate the amount og IGF-1 available

58
Q

How do IGF levels vary, are they connected to GH?

A

IGFs remain relatively constant over long periods despite fluctuations of GH

59
Q

What are the receptors of Gh? Which pathways can they lead to?

A

tyrosine kinases with adaptor proteins

Can feed into MAPK, IP3K, JAK/STAT

60
Q

What are the pathways IGF-1 receptor could lead to?

A

Acts via intrinsic tyrosine kinase activity, MAPK or IP3K

61
Q

What is the main difference- GH vs IGF receptors

A

IGF-1 has auto-phosphorylation activity - phosphorylation occurs instantly,

62
Q

What is the structure of IGF-1 receptor?

A

Similar to insulin receptor. Dimer of two glycoprotein subunits (AB)2

63
Q

What is the structure of IGF-II receptor?

A

Single-chain spanning the membrane once.

64
Q

What does IGF-11 bind also?

A

Also binds mannose-6-

phosphate.

65
Q

what is the IGF-II activity?

A

No known signal activity, at least postnatally

66
Q

WHat is the feedback controls of GH release

A

Balance between GHRH and somatostatin (GH release inhibiting hormone)
Feedback control by IGF-I on pituitary and hypothalamus
Feedback control by GH by acting upon GHRH
Control by the nervous system:
Control by metabolites

67
Q

GH release controls by the nervous system?

A
  • Stress (exercise, excitement , cold, anesthesia, surgery, hemorrhage) → surge in GH.
  • Sleep induces fluctuations in GH. Secretion every 1-2 h.
    Mental stress-> decrease in GH release levels
68
Q

How do metabolites affect GH release levels?

A
  • Increase: Hypoglycemia (e.g. produced by insulin administration); Amino acids (arginine)
  • Decrease: Hyperglycemia (oral glucose), free fatty acids
69
Q

GH release difference in adults vs young people

A

younger people have higher amplitudes of release and also more frequent releases

70
Q

balance between which 2 hormones determine GH release?

A

Balance between GHRH and somatostatin (GH release inhibiting hormone)

71
Q

GH vs IGF-1 concentrations through out development

A

GH concentrations go up, dip and come back up at adolescence, whereas the concentrations of IGF-1 parallel the body growth-> at 20 yo.o IGF concatenations go down

72
Q

GH and sex hormone interaction

A

GHR is. downregulated by GH or other factors (sex hormones)
Estrogens inhibit GH signalling by stimulating the expression of SOCS proteins which are negative regulators of cytokine receptor signalling.

73
Q

WHat are the causes of acromegaly?

A

Most cases of acromegaly are caused by a noncancerous (benign) tumor (adenoma) of the pituitary gland. The tumor secretes excessive amounts of growth hormone, causing many of the signs and symptoms of acromegaly

74
Q

Different Effect of glucose on GH levels in people with acromegaly vs normal

A

Normal: injection of glucose-> response from GH-> initial drop in GH levels followed by a gradual increase
increase in GH secretion
Acromegaly: GH levels stay constant and very high; levels of GH in acromegaly always exceed GH levels in a normal person

such response will not be observed if the patient already has a lot of GH such as in acromegaly
inject insulin -> observe the response
thus insulin tolerance and glucose tolerance tests are used for diagnosis

75
Q

GH response after insulin induced hypoglycemia: normal vs acromegaly

A

Normal: after insulin dose GH levels will surge

Acromegaly partial deficiency will be observed

76
Q

SOCS proteins are negative regulators of __ receptor signalling

A

SOCS proteins are negative regulators of cytokine receptor signalling

kris Endocrinology (17 decks)

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