Lecture #34 - Anterior pituitary e.g. growth hormone Flashcards Preview

HUBS191 - Module #3 - Endocrine System > Lecture #34 - Anterior pituitary e.g. growth hormone > Flashcards

Flashcards in Lecture #34 - Anterior pituitary e.g. growth hormone Deck (20)
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Compare and contrast the pituitary hormone secretion between ant and post lobe:

3 point for post and 4 points for ant


  • Neural input stimulates neurons in the hypothalamus (axon terminals in the posterior pituitary) to change action potential frequency.
  • Action potentials stimulate the release of specific stored hormones (ADH or oxytocin, made in the hypothalamus and stored at end of axons in post pit - BOTH PEPTIDE HORMONES) from the axon terminals in the posterior lobe into the circulation.
  • Released hormones travel in the blood to influence the activity of the target cells.



  • Neural input stimulates neurons in the hypothalamus to secrete releasing hormones (or inhibiting hormones).
  • Releasing hormones travel in the blood to the anterior lobe and bind to specific cell membrane receptors.
  • Hormone-receptor binding stimulates the cell to secrete specific stored hormones into the blood.
  • Released hormones travel in the blood to influence the activity of the target cells. 


The hypothalamus and the anterior pituitary gland 

1. What's the hypo connected to the anterior lobe by?

2. How does hypo communicate with ant lobe?

3. Ant pit hormones are made in the ___ __  by ___ ___

4. Hormone binds to _____ on _____ of a ____ ____ ____ and a _____ ____ ____ is secreted e.g. ?

1. The hypothalamus is connected to the anterior lobe by blood vessels

2. Hypothalamus communicates with the anterior lobe by hormones:-

•  releasing hormones

•  inhibiting hormones

3. Anterior pituitary hormones are made in the anterior pituitary by specific cells

4. Hormone binds to receptor on membrane of a specific cell type and a specific peptide hormone is secreted e.g. growth hormone, prolactin 


Anterior pituitary hormones

FSH and LH, GH, TSH, Prolactin and ACTH

All of these are produced within different cell types

What are their names? (5)

Endocrine cell - Hormone(s) - proportion of total anterior pituitary cell population 


1. Somatotrophs - Growth Hormone (GH) - 50%

-GHRH and SS stomatostatin control this so somatotrophs 

2. Mammotrophs (lactotrophs) - Prolactin - 20%

-Prolactin has major function of milk synthesis so mammary gland this mammotrophs

3. Corticotrophs - Adrenocorticotophic hormone (ACTH) - 20%

-ACTH stimulates release of cortisol from adrenal so corticotrophs 

4. Thyrotrophs - Thyroid stimulating hormone (TSH) - 5%

5. Gonadotrophs - Luteinzing hormone, Follicle-stimulating hormone (LH & FSH) - 5%

-Act on gonads so gonaotrophs


Anterior pituitary - 3 axis controlled by negative feedback

1. HPG axis 


Feedback regulation of anterior pituitary gland

Keeps hormone in good range 

Three levels of control here for each hormone (blue boxes)


Negative feedback regulation of prolactin - explain

1. WHat's the principal regulator?

2. PIH = ?

3. Prolactin stimulates what to inhibit prolactin secretion?

4. Positive or negative feedback?

5. What are the primary fuctions of prolactin?

-Prolactin is released from anterior pit and it is a nontropic hormone that goes and has a direct effect (doesn't act on another organ to have an effect)

-Prolactin RH on hypo acts on ant pit to release prolactin. If prolactin levels get too high, feedsback to another set of neurons called dopamine neurons (dopamine = prolactin inhibitory hormone- just another name like ADH or vasopressin) 

-Prolactin feeds back if conc gets too high and activates these dopamine neurons in hypo to release dopamine into median eminence and goes to ant pit and stops mamotrophs from producing prolactin. 

-So negative feedback system based on a different hormone (dopamine)

-So there's Prolactin hormone, PRH and PIH


  1. Principal regulator is prolactin inhibiting hormone (PIH)
  2. PIH is dopamine
  3. Prolactin stimulates PIH secretion to inhibit prolactin secretion
  4. Negative feedback!
  5. Prolactin has over 300 actions, including:-
    1. Stimulation of breast development
    2. Stimulation of milk synthesis 


Hormornal control of milk production 

1. Sensory info to hypo - sends something to post pit and milk ejected bc blood vessels contract or something 

2. Increase prolactin released and milk synthesis 




Regulation of growth hormone secretion

-This is the other NON-tropic hormone that is released from the ant pit that has direct effect (like prolactin)

-Has neurons that when stimulated release GHRH and when GH levels get too high, SS (somatostatin) neurons are activated (different set of neurons). SS neurons release inhibitory hormone to swtich off prodcution of GH if conc too high.

-If conc too low- GHRH neurons activated, Acts on somatotrophs and that releases GH. GH acts on the liver and it eleases insulin-growth-factor-1 (IGF-1). This negatively feedbacks on the GHRH neurons. 

-GH itself isn't the -ve feedback regulator - it's IGF-1

-If IGF levels become too high, it then acts on SS neurons to switch off GH release (acts on somatotrpohs to stop production of GH)

-So essentially; switch off neurons that're driving the GHRH and the same factor is stimulating release of inhibtor


Patterns of growth hormone secretion - daily 


It fluctutates 

-Pulsative secretion; neurons have bursts of activity so peaks throughout day but primary secretion during sleep (REM)


Patterns of growth hormone - gender


GH secretion 

  • Daily
  • Pulsatile
  • Gender difference 
    • Males; small burst during day and major burst during sleep 
    • Females; stronger/extended bursts during the day and longer (but not as pronounced) release during sleep
    • This is why sleep imporant bc that's when we get GH and GH helps to repair body and maintain tissue and has lotsa of effects on metabolism. 





Patterns of GH secretion - lifetime


  • GH concentrations are higher in children than adults with a peak period during puberty.
  • GH secretion declines with age in adulthood. 

-This is overall; it fluctuates daily

-Puberty it's the highest bc bones and organs etc growing




Patterns of growth hormone secretion – lifetime 

Girls go through puberty earlier than guys


What kinda hormone is GH?

a) peptide hormone

b) steroid

c) catechoamine 

d) thyroid 

It's peptide hormone 

-doesn't needa hv carrier protein bc it's water-soluble so dissolves in blood (does the whole receptor on membrane and cascade thing)

-lotsa hormones in body are peptide (75% of hormones)

-Has two dimers; two parts - forms the binding site for GH (v specific & recognises binding site on GH - nothing else fits)


Effects of growth hormone 

1. Growth effects (long-term)



2. Metabolic effects (short-term)



1. Growth effects (long-term)

-INDIRECT: stimulates the growth of bones, muscles and other tissues by stimulating cell division (mitogensis) via insulin-like growth factor (IGF-1)........therefore increase in GH in puberty. (IGF-1 peptides stimulate musles to be stronger so athletes take it? Has no signifcant effect on a healthy indivisual)

-DIRECT: stimulates protein synthesis (in muscle)........GH binds to receptor in muscle cell and protein synthesis initiated in myocyte so stronger


2. Metabolic effects (short-term):

-DIRECT: increases blood glucose by stimulating glucose synthesis (in liver) and inhibiting cellular uptake of glucose.......Make glucose from aa' and GH stimulates the making of glucose so stops taking up of glucose from blood stream - allows skeletal muscle to bc more active 

-DIRECT: increases triglyceride breakdown and free fatty acid mobilization in adipose tissue.......breaks down fat source & they can be used for energy for muscles (skeletal) - same with glucose above




Endocrine disorders associated with growth hormone 

1. Two types - what are they?

2. Growth hormone

-three parts

3. Hormome receptors

-two types 

1. Two types:

  • Hyposecretion: too little (or none)
  • Hypersecretion: too much
    • Something is wrong in the hypo axis 


2. Growth hormone 

  • Deficiency (dwarfism) - not enough development during puberty
  • Excess (gigantism)
  • Normal levels 


3. Hormone receptors 

  • Hyposensitive: little response (or no) response
    • Something wrong in receptors and can no longer respond to it - no ligand binding site or mutation somewhere in sequence and can't bind
  • Hypersensitive: respond too much 
    • Doesn't even need GH there - just always switched on 



Endocrine disorders; acromegaly 

  • Excess GH in adulthood leads to thickening of bones, soft tissues of hands, feet and face 


Acromegaly - twins

Growth and acromegaly in one individual of a pair of identical twins

-share same DNA but mutation occurred


Other hormones important for growth (4)

  • Thyroid hormone
    • increases basal metabolic rate
    • essential for nervous system development (cretinism - shown in picture)


  • Insulin
    • glucose metabolism (energy substrate for growth)


  • Cortisol
    • glucose metabolism


  • Testosterone/estrogen
    •  essential for puberty (onset won't start if none of this)


Tropic and non-tropic hormes

Tropic - have stimulating effects on other endocrine glands. These hormones stimulate the developement of their target glands and tend to stimulate synthesis and secretion of target hormone



-FSH and LH


Non-tropic are prolactin and GH