Growth Hormone (9) Flashcards

1
Q

What type of hormone is GH?

A

Peptide hormone

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2
Q

Where is GH produced?

A

Anterior Pituitary

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3
Q

What two regulation factors does the hypothalamus produce? What are their effects?

A

GHRH: stimulates

Somatostatin: Inhibitory

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4
Q

What factor does the stomach and pancreas secrete that regulates GH?

A

Ghrelin

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5
Q

What does the integration of GHRH and somatostatin result in?

A

Episodic, pulsatile secretion

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6
Q

What are the effects of GHRH (name 4)?

A

1- increased GH gene transcription

2- Promotes GH release

3- Stimulates production of GHRH receptor

4- Stimulates somatostain release

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7
Q

What are the effects of Somatostain (name 4)?

A

1- Decreasespulse frequency

2- Decreases pulse amplitude

3- No impact on GH synthesis

4- Inhibits GHRH release

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8
Q

When do growth hormone pulses mainly occur?

A

At night at higher frequencies

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9
Q

What do the following factors allow for?

Deep sleep, exercise, sex steroids, hypoglycemia, amino acids, stress, dopamine agonists

A

Stimulate GH secretion

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10
Q

What do the following factors allow for?

IGF- I, Obesity, glucocorticoids, hyperglycemia, free fatty acids, GH, beta- adrenergic agonists

A

Inhibition of GH secretion

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11
Q

What doe increased levels of GH and IGF-I do to somatostatin release?

A

Increase somatostatin release

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12
Q

What doe increased levels of GH and IGF-I do to GHRH release?

A

decrease GHRH release

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13
Q

What type or receptor does GHRH bind to?

A

Gs protein coupled receptor on somatotrophs

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14
Q

When GHRH binds its receptor, what are the effects within the cell?

A

1- increased cAMP which activates PKA to Phosphorylate CREB…which then augments Pit-1 a transcrption factor that upregulates GH and the GHRH receptor

2- increased Ca++ which leads to secretion of GH

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15
Q

What type of receptor is the GH receptor?

A

Transmembrane receptor of the cytokine family

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16
Q

Where are the major sites of action of GH receptors?

A

Bone, Liver, Adipocyte, Muscle

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17
Q

What pathway do receptors for GH activate?

A

JAK/ STAT pathway of signal transduction

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18
Q

Do GH receptors have inherent tyrosine kinase activity?

A

No

19
Q

What does the binding of GH to its receptor cause?

A

receptor dimerization and binding of a JAK tyrosine kinase

20
Q

What do activate JAKS do?

A

Phosphorylate the STATs, which as dimers translocate to the nucleus and act as trascription activators

21
Q

What are the effects of GH on the liver?

A

production of IGF-I and stimulateshepatic glucose production

22
Q

What are the effects of GH on the adipocytes?

A

Stimulates the release and oxidation of free FAs by the reduction of the activity of Lipoprotein lipase

Lipogenesis is reduced

23
Q

What are the effects of GH on skeletal muscle?

A

anabolic actions on skeletal muscles…stimulates amino acid uptake and incorporation into proteins and suppresses protein degradation

24
Q

What are the effects of GH on the brain?

A

Affects mood and behavior

25
Q

What are the effects of GH on bone?

A

differentiation of prechondrocytes into chondrocytes

26
Q

True or False:

GH induces growth in animals that lack insulin

A

false

27
Q

What is primarily sued for screening when considering GH deficiencies?

A

IGF-I (because levels are more stable and not cyclic)

28
Q

How do Insulin, IGF-I and IGF-II resemble one another?

A

all have A, B and C domains which share a high degree of AA sequence homology

29
Q

What additional piece do IGF-I and IGF-II have when compared to insulin?

A

D domain

30
Q

What happens when the IGF-I recepter dimerizes?

A

Autophosphorylation of the receptor recruits IRS-1 and Shc

31
Q

What happens when IRS-1 and Shc are phosphorylated by the IGF-I receptor?

A

they recruit other proteins to the membrane which then activates the PI3-inase and Ras/MAP kinase pathways.

Both of these pathways regulate cellular transcription

32
Q

What plays a large role in the growth spurt during puberty?

A

sex hormones

33
Q

What is the cause of Laron Syndrome?

A

Point mutation or deletion in IGF receptor that causes low IGF-I concentrations and normal/ elevated GH concentrations

34
Q

What is Laron syndrome treated with ?

A

rhIGF-1

35
Q

What can gigantish lead to?

A

hyperglycemia —-> diabetes mellitus due to degradation of beta cells in the pancreas

36
Q

What causes acromegaly

A

Growth hormone secreting adenomas

37
Q

What are the anatomical characteristics of Acromegaly?

A

protrusion of the jaw, enlarged tongue, enlarged hands and feet, carpal tunnel syndrome, reduced strength

38
Q

What are the implications of GH deficiencies for cardiovascular disease?

A

Increases visceral adipose tissue and decreased myocardial function

39
Q

What happens to GH as a person ages?

A

Levels decrease and this contributes to some normal effects of aging…like loss of muscle mass and increased interstitial body fat

40
Q

What is GH approved to treat?

A
Gh deficiency
Idiopathic short stature
Turner syndrome
Prader-Willi syndrome
Chronic renal insufficiency
Small for gestational age
41
Q

If you have celiac disease, how is your IGF-I level affected?

A

Reduced levels because if nutritional deficiencies related to the disease

42
Q

What is the short stature in Turner syndrome attributed to?

A

Haplonoinsufficiency of the SHOX gene because of an absence of an X chromosome

43
Q

What are the most common genetic syndromes that cause short statures in the US?

A

Turn and Down sundrome

44
Q

How is the SHOX protein regulated?

A

It is developmentally regulated. It is expressed throught the fetak growth plate but is most concentrated in the hypertrophic zone during childhood