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endocrinology Flashcards

1
Q

a) What is the function of the hypothalamus and b) where is it located?

A

a) Regulates and coordinates responses to changes in the external and internal environment
b) The surrounding walls of the 3rd ventricle in the brain, posterior to the optic chiasm

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2
Q

What is the structure of the hypothalamus?

A

Made up of several nuclei containing cell bodies and nerves containing axons that project to the pituitary.
- nuclei include PVN and SON

Made up of Neural Tissue and Endocrine Gland

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3
Q

What is the body’s physiological response to hormones?

A

The uptake in the blood (lipid-based) hormones which are bound to plasma proteins; or direct uptake into target cells (hydrophilic hormones) or metabolism preceding secretion.

The Response Process

  • Endocrine gland (Ant. Pituitary) secretes hormone
  • Hormone (peptide chain – signal) is either free, biologically active or bound to plasma proteins (lipophilic hormone)  recognised by the target cells; OR
  • Some are metabolised in the liver/other tissues  then recognised by target cells; OR excreted in urine (inactivated before excretion)
  • Target cells (dependent on sensitivity) induce a physiological response.
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4
Q

What 2 factors is physiological response to hormones dependent on?

A
  1. Concentration of hormone (free, biologically active fraction)
  2. Sensitivity of target cell receptors
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5
Q

What is the connecting structure known as between the hypothalamus and the pituitary and what does it contain?

A

The Pituitary Stalk / Infundibulum

Contains axons from the PVN and SON that act on the ant. and post. pituitary gland. that traverses the median eminence.

Contains the hypophyseal portal system.

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6
Q

What does the Hypothalamus regulate?

A

Behaviours including…

  • Reproduction
  • metabolism (body mass, rate, hunger/satiety)
  • body temperature
  • water balance (retention)
  • growth
  • stress
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7
Q

What are the general steps involved in hypothalamic regulation?

A

Input (neural humoral) –> Hypothalamic integration –> Output (neural humoral)

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8
Q

What are the 2 endocrine gland output sites of the Hypothalamus?

A 
Anterior Pituitary (adenohypophysis)
Posterior Pituitary (neurohypophysis)
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9
Q

Posterior Pituitary gland is regulated by what structures?

A

Being a neurohypophysis gland, it is responsive to the axonal connections from the hypothalamus particularly the PVN and SON (magnocellular neurones)

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10
Q

What are the 2 neurohormones the Post. Pituitary stores and secretes? Where are they secreted?

A

ADH (vassopressin) and Oxytocin

Nerve dendrites interact with nerve terminals at the capillary bed and release the neural humoral response directly into the blood stream.

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11
Q

What is the role of ADH (vasopressin)? What regulates its secretion?

A

Anti-Diuretic Hormone (ADH) reulgates the water balance in the body by increasing water retention in the kidneys (decreasing water excretion). It also innervates arterioles for vasoconstriction to increase BP.

Secretion is regulated by the ECF by osmoreceptors and the Blood Volume by the right atrium stretch receptors.

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12
Q

What is the role of Oxytocin in the human body?

A

stimulates the smooth muscle of uterine walls during parturition
helps with the ejection of milk during breastfeeding by contracting smooth muscle = Lactation

  • known as the cuddle hormone
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13
Q

What stimulates oxytocin secretion and inhibits it?

A

Secretion = suckling baby on nipple; pressure from baby in birth canal

Upregulation of OT expression
• During pregnancy via oestrogen
• Maintained by suckling stimulus

Inhibition = fear, anxiety

influenced by optic and auditory inputs!

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14
Q

What are the target cells of oxytocin?

A

The smooth muscle below basal membrane of alveolar epithelial cells = Myoepithelial cells (expressing oxytocin receptors)

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15
Q

Pathway of Oxytocin synthesis, passage and release:

A

Synthesis = biosynthesis in cell body –> transcription, translation, packaging, and glycosylation

Passage = Processing and axonal transport through dibasic cleavage, single base cleavage, carboxy peptidase, and amidation

Release = OT release together with NP into bloodstream; storage for exocytotic release, and membrane recapture

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16
Q

Describe the Oxytocin signal transduction into myoepithelial cells.

A
  • Oxytocin binds to a G-protein coupled receptor (OT-R) attached (Ga(q)), signals through Phospholipase C (PLC)
  • This then causes PIP2 to release signalling from IP3; IP3 binds to IP3 Receptors on the SR or ER to act as a channel for Ca2+ fluxes out into the cytoplasm (from SR or ER) to stimulate actin/myosin cross-bridge formation (Phosphorylation of myosin)
  • Ca2+ is taken up again to prepare for the following signal  Ca2+ from the extracellular space also enters the cell through Ca2+ channels to help with this contraction.
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17
Q

What hormones are secreted in the Anterior Pituitary?

A 
Gonadotrophs - LH and FSH
Somatotrophs - GH
Corticotrophs - ATCH
Thyrotrophs - TSH
Lactotrophs - Prolactin
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18
Q

Describe the transduction of signals to releasing hormone to ant. pituitary hormone release and it significance of the median eminence.

A

Releasing factors (or releasing hormones)
• secreted from nerve endings into capillaries at
specialised region of hypothalamus = “median
eminence”
• transported in hypophyseal portal circulation to a second
capillary bed in the anterior pituitary gland.
• act on their target cells to stimulate synthesis
and secretion of the anterior pituitary hormone

eg. GHRH from median eminence to the GH release from Ant Pituitary.

releasing factors are small peptides (3-40 residues long)

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19
Q

True or False: Activity of each cell type is regulated independently of the others.

A

True - due to the presence of individual releasing factors

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20
Q

What is the clinical relevance of a HYPOTHALAMO-PITUITARY DISCONNECTION?

A

All hormone concentration decreases EXCEPT for Prolactin where it increases!

This is due to GH, ACTH, TSH, LH/FSH are all under Excitatory Control thus when a stalk section occurs, there is no more stimulus for release. On the other hand, Prolactin increases as it is under Inhibitory control thus when the stalk section occurs, inhibitory activity on Prolactin stops and allows for excitatory activity to occur, increasing its release!

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21
Q

Name and list the RF and RIF for the ant. pituitary hormones.

A

Prolactin: RF = ? ; RIF = Dopamine

ACTH: RF = CRH ; RIF = ?

LH/FSH: RF = GnRH ; RIF = GnIH

TSH: RF = TRH; RIF = none.

GH: RF =GHRH ; RIF = Somatostatin

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22
Q

Beginning with the endocrine gland, what is the sequence of events that leads to a physiological response to a hormone within a cell?

A

Endocrine gland secretes its hormone (eg. GH) into the blood system (either free biologically active or, when inactivated, bound to a plasma protein) then will bind to the target cell receptor (GPCR). This then triggers the G-protein cascade into the cell and the cell’s nucleus to alter genes to express desired physiological response on the effector cell (eg. GH on the liver).

  1. The endocrine gland secretes the hormone into circulation.
  2. Within the plasma, some of the hormones are bound to plasma proteins in an inactivated, while some are free and biologically active.
  3. Hormones in the blood is circulated to target cells, bind to hormone specific receptors.
  4. Receptor activation results in a physiological response.
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23
Q

How does the hypothalamus function as an integrative centre?

Refer to the inputs, integration and outputs in your answer

A

The hypothalamus receives neural input from the body’s sensory modalities (sight, smell, sound taste, touch, thermoreception).
It also receives humoral input from systemic circulation (e.g. blood sugar levels, hormones).
After integration and processing, outputs from the hypothalamus could occur via neural (directly synapsing other nerves, like to brainstem and down spinal cord to tissues) or humoral (hormones secreted into circulation and act on anterior pituitary gland).

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24
Q

True or False: There are more cells in the Ant than Post Pituitary

A

True

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25
Q

What are the five cell types in the Ant. Pituitary and their corresponding hormone they produce?

A 
Somatotrophs - GH
Corticotrophs - ACTH
Gonadotrophs - LH/FSH
Thyrotrophs - TSH
Lactotrophs - PRL
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26
Q

What are the features of the capillaries of the Ant. Pituitary gland?

A

Fenestrated Capillary - characteristic of Ant. Pituitary which allows for the passage of small proteins such as hormones to pass through.

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27
Q

True or False: The presence of separate axes between cells and hormones allows for functional separation.

A

True

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28
Q

How does the Ant. Pituitary enhance endocrine communication via its capillaries?

A

The capillaries of the anterior pituitary gland have a fenestrated structure. This structure allows hormones and other large macromolecules to cross from blood into interstitial space more readily than if the capillaries had a normal continuous capillary structure, where the capillary endothelial cells are tightly joined. The result is faster delivery (diffusion) of hormones from/to the capillaries for both releasing factors from hypothalamus and anterior pituitary hormones. Remember most of these hormones are polypeptides or small proteins. Therefore, the fenestrated capillary structure enhances cell communication.

29
Q

What are the Anterior Pituitary Hormones predominately regulated by?

A

Releasing Hormones/Factors

eg. GH regulated by GHRH

30
Q

Describe the Pathway of Hypothalamic regulation on ACTH release in the adrenal cortex, include structures and hormones involved.

A

The hypothalamus receives stress stimuli from either external or internal environments and triggers a signal from the associated nuclei to adapt to the stressor. The signal travels to the median eminence where, at the junction between nerve terminals and the hypophyseal portal system, it becomes a chemical releasing factor for ACTH, specifically CRH (corticotrophin releasing hormone) which then travels through the hypophyseal portal system rostrally and entering the anterior pituitary’s capillary bed. Due to the fenestrated nature of the anterior pituitary’s capillaries, CRH is able to pass through to the target cell, corticotroph, to stimulate it to synthesis and release the hormone ACTH. This then is incorporated into the bod’s systemic circulation and acts on the adrenal cortex where it produces cortisol in response to the stress.

  1. Neurosecretory cells in the hypothalamus secrete corticotrophin releasing hormone (CRH) from the nerve endings into capillaries at specialised region of the hypothalamus known as the median eminence.
  2. The releasing factor, CRH, is transported via hypothalamic-hypophyseal portal and binds to receptors on corticotrophic cells in the anterior pituitary gland.
  3. Upon stimulation by CRH, corticotrophs synthesise and secrete ACTH into peripheral circulation. 4. ACTH travels via the circulation to the adrenal gland. ACTH binds to receptors in the adrenal cortex to stimulate the synthesis and secretion of cortisol.
31
Q

Explain the steps involved for the Ant, Pituitary hormones from release in the hypothalamus to the release of the hormone in the effector organ. Include structures and hormones.

A

write one description for each…

32
Q

a) How is the hypothalamus connected to the posterior pituitary gland?
b) Where is the site of synthesis and secretion of the posterior pituitary neurohormones oxytocin and vasopressin?

A

A) The connection between the hypothalamus and pituitary gland is called the pituitary stalk. There is a neural connection between the hypothalamus and posterior pituitary gland. Axons of hypothalamic neurons run down the pituitary stalk to the posterior pituitary gland. B) Synthesis occurs at the cell bodies located in hypothalamic nuclei, in particular the PVN and SON, whilst secretion is from the nerve terminals in the posterior pituitary into capillaries.

33
Q

What are the physiological effects of ADH?

A

Increase Blood volume / pressure
Exert anti-diuretic effects on body (kidneys)
Decreases plasma osmolarity

34
Q

What is the function and target cell of oxytocin?

A

Oxytocin stimulates the contraction of smooth muscle at the myoepithelial cells to facilitate milk ejection.
–> stimulated by baby sucking on nipple

Oxytocin also assists in parturition as the pressure of the baby in the birth canal facilitates smooth muscle contraction in the uterine wall.

It is also involved as a trust forming hormone.

35
Q

Describe oxytocin signal transduction.

A

Oxytocin binds to OT-R which is a g-protein coupled receptor (GPCR) which signals through the Gq protein.

This Gq protein signal divides PIP2 into 2 compounds 1. DAG and 2. IP3 through activation of PLC.

IP3 then is able to bind to the ER or SR of the Myoepithelial cell presenting IP3 receptors, which is a Ca2+ channels, to induce a transient influx in Ca2+ in the cell.

This Ca2+ influx is paired with another transient Ca2+ increase through the CICI (calcium induced calcium influx) which facilitates the myosin phosphorylation to form cross-bridges and thus cause smooth muscle contraction.

Step 1: Oxytocin binds to oxytocin receptors (a GPCR) on the plasma membrane of the myoepithelial cell:

Step 2: Activated Gq proteins act via Phospholipase C (PLC), which converts PIP2 into IP3 and DAG.):

Step 3: IP3 acts on IP3-Receptors which are Ca2+ channels to release of stored calcium from the ER/SR:

Step 4: Ca2+ acts on contractile proteins, generating contractile force in the myoepithelial cells:

36
Q

What is the process by which milk is ejected during lactation?

A
  1. Suckling of the breast is detected by mechanoreceptors and relays signals to the spinal cord.
  2. Neural signals are relayed to the paraventricular (PVN) and supra optic nuclei (SON) of the hypothalamus.
  3. Oxytocin are activated ie depolarised. 4. Oxytocin is released, synpatic vesicles release, into capillaries within the posterior pituitary gland 5. Oxytocin circulates and acts a hormone on the myoepithelial cells in the breast 6. Contraction the myoepithelial smooth muscle causes milk in the milk ducts to be ejected.
must refer to:
Mechanoreceptors in the breast
Neurons in the hypothalamus
Stimulation of oxytocin secretion
Myoepithelial cells
37
Q

Describe the process by which prolactin is spontaneously secreted from lactotroph cells?

A

In the absence of dopamine the PIF, the lactotroph cells spontaneously secrete prolactin. However normally dopamine is present and there is a suppression of prolactin release from the lactotroph cells.

In the absence of dopamine, inside the lactotroph cells ATP is converted into cAMP (via adenylate cyclase), cAMP accumulation is coupled to membrane depolarization and opening of the voltage gated Ca2+ ion channels, causing Ca2+ influx. High intracellular Ca2+ promotes vesicles fusion and exocytosis of prolactin from the lactotroph cells. Hence, prolactin is spontaneously released.

38
Q

What impacts does DOPAMINE have on secretion, synthesis and lactotroph proliferation?

A

Secretion: short term decrease response through the mechanisms of blocking secretory function of cells and PRL

Synthesis: mid-term decrease response of produce of PRL mRNA

Lactotroph Proliferation: long-term response to dopamine ie. cell size of lactotroph - clinically relevant in tumours of pituitary etc.

39
Q

What happens to the lactotrophs and secretion of PRL when dopamine is removed?

A

Spontaneous Prolactin secretion from lactotrophs.

AC and its subsequent cAMP drives PRL secretion via exocytosis

  1. cAMP signals to voltage gated Ca2+ channel to increase intercellular Ca2+ by changing membrane permeability and causing depolarisation
  2. This presence of Ca2+ in cell facilitates vesicle fusion with PRL to allow exocytosis of PRL out into the interstitial fluid.
  • Increase cAMP
  • Membrane depolarisation
  • Influx of Ca2+
  • Promotes prolactin release via Exocytosis
40
Q

How does Dopamine inhibit PRL secretion form lactotrophs?

A

Dopamine inhibits many stages of spontaneous PRL secretion.

D2 receptor binds with dopamine; being a Gi G-protein couple receptor, it therefore inhibits the conversion of AC to cAMP which in turn prevents transient Ca2+ influx into the cell and a lack of depolarisation due to less ATP present in the cell. As a result, you get less exocytosis or less secretion of PRL in the short-term.

41
Q

Describe the control of synthesis of PRL in a non-lactating individual.

A

Dopamine a neurohormone is tonically released from the hypothalamus. Prolactin stimulates this dopamine release via feedback.

  • Dopamine is the release inhibitory factor for prolactin and prolactin via short loop negative feedback enhances dopamine release)} ( ) Prolactin and dopamine activation of dopaminergic neurons upregulates downstream synthesis and secretion of prolactin by lactotrophs {{Incorrect. Prolactin activation of dopaminergic neurons will increase dopamine release, which will DOWNREGULATE downstream synthesis and secretion of prolactin by lactotrophs
42
Q

Describe the change in the robustness of PRL release during sucking of the nipple and once the baby has stopped. What is the purpose of this change?

A

There is a robust increase in the PRL concentration in early lactation. Once sucking from baby has stopped, there is less secretion of PRL in the blood, this has a waning effect to allow for a second signal to induce further feeding in the future.

early versus mid lactation is in early lactation the prolactin
increases rather robust compared to mid lactation.
So in other words the effect wanes over time.

43
Q

What are the hormones responsible for the action of breastfeeding?

A

dual control around lactation in both involves the hormone
prolactin as well as the hormone oxytocin.
The interesting thing is the mechanoreceptors sucking on
the nipple affixed both oxytocin secretion from the posterior
pituitary as well as prolactin secretion from the anterior
pituitary. Remember that oxytocin is involved in milk ejection
responses and contraction of the smooth muscle in the breast
tissue where as prolactin stimulates milk synthesis and
secretion by the epithelial cells but the regulation
involves both hormone.

44
Q

Describe the order of events involved in milk production when a baby suckles in lactation.

A

Step 1: Suckling induces activation of mechanoreceptors in the nipple, with a neuronal relay to the hypothalamus

Step 2: There is a decrease in the release of dopamine from the median eminence; increase in oxytocin release from post. pituitary

Step 3: Increased release of prolactin from the lactotrophs

Step 4: Increase in milk secretion by alveolar epithelial cells

Step 5: Increased milk ejection through the nipple

45
Q

What time of negative feedback loop does the PRL hormone have to inhibit the PRL in non-lactating individuals? How does it function?

A

Short Negative feedback loop. Maintains low PRL in non-lactating individuals.

Since prolactin does not stimulate the breast or mammary
gland to produce a hormone; We don’t have long loop (-) feedback.

Short feedback = When the endocrine cell WITHIN anterior pituitary loops back to hypothalamus to further inhibit release of the hormone.

Long feedback = When the endocrine gland secreting the hormone (not releasing factor) loops back to the Anterior Pituitary and the Hypothalamus to inhibit release of the target hormone.

The Dopaminergic neurons detect the presence of PRL in the circulating blood (through the BBB) via receptors on these neurons. this then causes these neurons to sustain/increase firing of DOPA neurons and dopamine into the anterior pituitary. As a result, the lactotroph’s dopamine receptors (D2) bind with dopamine from hypophyseal portal blood to further inhibit PRL release from lactotrophs and the cycle continues. (ie. prolactin, by binding to these PRL-R receptors, stimulate dopamine synthesis and secretion into hypophyseal portal blood, further inhibiting PRL)

46
Q

What is the target cell/enzyme in PRL-R Signalling at the Dopaminergic neurons in the hypothalamus? Describe the signalling pathway and the end point.

A
  1. The PRL is accepted by the PRL-R
  2. JAK2 (Janus kinase-signal transducer) binds to PRL-R and is phosphorylated.
  3. This induces the binding of STAT5 as JAK2 phosphorylates the STAT5 binding site.
  4. STAT5 is then phosphorylated by JAK2 which triggers STAT5 to form a dimer and undergo nuclear translocation (enter nucleus of cell - nerve cell).
  5. The difference here is that STAT5 dimer binds to STAT response elements on the DNA promoter regions of genes where one of its key targets in the dopamine neurons in the hypothalamus is tyrosine hydroxylase.
    - Tyrosine hydroxylase is a rate limiting enzyme for catecholamine synthesis (ie. dopamine synthesis).
  • In other words, what prolactin does is signal to the dopamine neurons to switch on the production of tyrosine hydroxylase
    which then acts as an enzyme to stimulate dopamine synthesis which IN TURN inhibits further PRL synthesis and secretion.
47
Q

What happens to the PRL signal transduction in Lactating individuals? ie. How does PRL synthesis get stimulated and released into mammary tissue to produce milk for breast feeding?

A

When circulating prolactin passes through the BBB to bind to PRL-R on dopamine releasing neurons in the Hypothalamus. Inhibiting factors, called SOCS1,2,3 (and CIS) interfere with JAK-STAT signalling through binding to Phosphorylation sites and therefore down regulate receptor response.

This prevents STAT dimer formation, Nuclear translocation and therefore, tyrosine hydroxylase from promoting Dopamine synthesis!

This process causes an Insensitive or Resistance state to PRL

Less Short loop negative feedback due to CIS (SOCS protein) causing PRL insensitivity and downregulation of Dopamine!

48
Q

Explain the underlying physiological mechanisms that result in hyperprolactinemia in lactating women.

A
  1. Sucking of nipple by baby stimulates mechanoreceptors
  2. Sensory neuronal feedback via spinal cord to hypothalamus
  3. Inhibition of the dopamine neurons in the hypothalamus that regulate PRL
  4. Beside inhibiting depolarization and dopamine release, there is an increase in SOCS proteins that desensitise the dopamine neurons to PRL short loop negative feedback (main SOCS protein is CIS)
  5. There is a down-regulation of the rate limiting enzyme tyrosine hydroxylase for dopamine synthesis
  6. Overall less dopamine synthesised and released at the median eminence
  7. Since there is less dopamine there is less inhibition of the lactotrophs, so more spontaneous PRL release
  8. At the same time, the sucking stimulus input into the hypothalamus stimulates the release of the Prolactin releasing factor whose identity is unknown. This PRF is released into hypophysial portal blood and stimulates PRL release from lactotrophs. Altogether the above mechanisms increase blood levels of prolactin (hyperprolactinemia) in lactating women.
49
Q

Describe Patho physiologies associated with Prolactin.

A

Females:
Hypersecretion = (usually due to adenoma –> Prolactinoma)
- Causes inappropriate milk production GALACTORRHEA.
- Causes decrease in fertility Lactoral AMENORRHEA
Hyposecretion = Poor synthesis and secretion of milk in breast tissue.

Males:
Hypersecretion = due to Prolactinoma (tumour of the lactotroph in Ant. pituitary.
- Causes breast development and possible milk production GYNECOMASTIA
- Causes the turning off of the hypothalamus pituitary gonadal axis and thus get less testosterone production and therefore low libido in males.
Hyposecretion =

50
Q

What is the pattern of distribution of hGH pulsation (human GH) in males and females?

A

Men have less frequent, greater amplitude pulsation throughout the day ie, more pulsatile

Women have more frequent, less amplitude pulsation throughout the day ie, more continuous

This dimorphism is significant in metabolism in the liver

Males have a greater amplitude of GH and infrequent pulses. Females have smaller amplitudes but more frequent, continuous pulses. However, both males and females roughly have the same area under the curve (integrated GH), outlining that the total amount of GH is secreted is similar in value. You will explore this area more in the laboratory practical.

51
Q

Describe the process of Somatostatin decreasing GH concentration in the body via the short negative feedback loop.

A

GHRH is released from hypothalamus stimulates the release of GH from the somatotrophs in the anterior pituitary gland. In contrast somatostatin from the hypothalamus inhibits Gh secretion.
Circulating GH crosses the blood brain barrier to bind to GH receptors on both GHRH and somatostatin neurons in the hypothalamus.
GH through short loop negative feedback, inhibits the activity of GHRH neurons whilst stimulating GH release inhibitory neurohormone, somatostatin.
By decreasing a releasing factor GHRH and at the same time increasing a release inhibiting factor somatostatin, these together result in a decrease in GH synthesis and secretion, lowering blood GH concentrations Somatostatin acts on the anterior pituitary gland, regulating lowering GH secretion.

52
Q

What are the direct actions of GH-R

A

Muscle - increases muscle mass

  • -> increases aa uptake
  • -> decrease glucose uptake
  • -> decrease protein degradation

Adipose Tissue - decreases fat deposition

  • -> decrease glucose uptake
  • -> increase fat tissue breakdown

Liver - increase overall blood glucose

  • -> increase protein synthesis
  • -> increase gluconeogenesis
53
Q

What effect does GH and IGF-1 have on cells?

A 
GH = cell proliferation
IGF-1 = cell hypertrophy
54
Q

What is the effect of GH in a developing child vs an adult?

A

Open epiphysis in Development = true growth + metabolic effects
metabolic effects –> increase blood glucose (anti-insulin)
–> increase lipolysis (anti-insulin)
–> increase protein synthesis; decrease protein catabolism

Close Epiphysis in adulthood
= maintained metabolic effect +muscle mass

55
Q

i) How does Growth Hormone stimulate stature (lengthening of long bones)? In your answer, include important terms such as; proliferation, chondrocytes, hypertrophy, GH, IGF-1).
ii) After growth plate closure, how does the GH/IGF-1 axis affect the growth of bones?

A

i) At the epiphyseal growth plate in long bones (the site of bone growth), GH & IGF-1 act together to increase length. GH induces hyperplasia of chondrocytes ie. increasing proliferation of chondrocytes. IGF-1 stimulates the hypertrophy of chondrocytes in long bones ie. increasing cell size which also contributes to lengthening the bone

Extra that you might include here a) Whilst GH comes from the somatotrophs in the anterior pituitary gland, IGF-1 can be derived from the liver (somatomedin axis) or importantly in long bone growth IGF-1 is synthesised within chondrocytes. GH receptors ar abundant on chondrocytes and IGF-1 produced acts locally to promote cell hypertrophy. b) The epiphyseal growth plates on long bones close soon after puberty due to estrogen action, and GH cannot further increase the length of bones, only the thickness - thus chondrocytes can still respond to IGF-1.

56
Q

i) How does GH affect protein synthesis?

A

iii) GH is protein anabolic. It decreases the rate of protein breakdown in cells. Together with insulin it promotes amino acid uptake into myocytes/muscles. In the liver GH promotes protein synthesis.

57
Q

Compare the short and long negative feedback loop for GH.

A

Comparable: The ultimate control of GH is at the hypothalamic level through either the releasing factor GHRH and the release inhibitory factor somatostatin. Both short loop and long loop negative feedback act act on the hypothalamus to regulate these neurons. Contrasts” Short-loop negative feedback is via GH itself acting on the hypothalamus. GH stimulates somatostatin neurons whilst it inhibits GHRH neurons. In contrast, long loop negative feedback involves IGF-1 mainly from liver, acting at both the hypothalamus like GH short-loop feedback but also at the anterior pituitary gland acting on somatotrophs to regulate their response to hypothalamic control via GHRH and somatostatin.

58
Q

The hypothalamus receives information about internal and external environments such as hormone levels, metabolic levels, stress, exercise and sleep.

How does the hypothalamus integrate the information from these internal and external environments to modulate the release of growth hormone?

A

By taking in information from multiple internal and external stimuli, the hypothalamus integrates the information to determine whether it is appropriate to release GHRH or somatostatin and how much of these hormones are released. These hormones then travel to the anterior pituitary gland to either enhance (GHRH) or reduce (somatostatin) the release of growth hormone. In this way, the hypothalamus can modulate the amount of growth hormone under different circumstances faced by the body at different times.

59
Q

What are the other hormone required for effective normal growth with GH?

A

Permissive role hormones for GH:

  • Thyroid hormone
  • Glucocorticoids
  • Sex steroids (t and e)
  • insulin
60
Q

Explain Arcomegaly as a GH deficit in adulthood.

A

A hypersecretion of GH which increases the size (hypertrophy) of extremities (hands) and bone lengthening and of mandible (face).

Enlargement of soft tissues at leads to malformation, tongue, lips, deep voice

Generally caused by a pituitary tumour

61
Q

Explain the deficit of Gigantism

A

The excessive GH in childhood, hypersecretion. Soft tissues are also effected (heart, lungs).

All body parts are in proportion

62
Q

What does a GH deficiency cause?

A 
Pituitary Dwarfism In Children
--> normal body proportions
--> short stature
--> poor muscle development
--> excess subcutaneous fat
No effect noted for Adults
63
Q

Compare and contrast the consequences of growth hormone excess in children and adults?

A

COMPARABLE GH excess in children and adults is usually due to hypersecretion of GH from somatotrophs. CONTRASTS In children excess Growth Hormone will cause excessive growth and lead to gigantism as the epiphyseal plates on long bones are still open ie. responisve to GH. However, soft tissues will still be in proportion. In adults, excess Growth Hormone leads to acromegaly where individuals display enlarged extremities, including the hands, feet and face. There is no increase in stature.

64
Q

Describe the relationship between early growth and IGF-1

A

During periods of high correct growth velocity, such as the first few years of life and during puberty, Growth Hormone is critical in promoting growth. However during puberty IGF-1 concentrations
increase correct and this aids in the pubertal growth spurt. Blood IGF-1 concentrations are low during the first 5 years of life correct , because the somatotrophic (GHRH-GH-IGF1) axis is not mature. After puberty into adulthood pulsatile GH decline and similarly there is a decline in circulating IGF-1.

65
Q

Describe the Somatomedin hypothesis

A

The hypothalamus releases pulsatile GHRH which stimulates the synthesis and secretion of pulsatile GH from the somatotrophs and in turn GH acts on the liver. GH binds to GH-receptors on hepatocytes to stimulate IGF-1 secretion that mediates growth effects on somatic cells.

66
Q

How do growth hormone and insulin-like growth factor-1 (IGF-1) work together to control somatic growth?

A

The anterior pituitary gland releases growth hormone which acts to stimulate IGF-1, primarily from the liver (somatomedin hypothesis) but also in other tissues. IGF-1 can act as a classical hormone, circulating and binding to target tissues to induce somatic cell growth. Also IGF-1 can act in a paracrine manner to stimulate local growth in tissues. Some local IGF-1 may enter circulation (“spill-over”) and contribute to the circulating IGF-1 pool and affect somatic cell growth elsewhere in the body. Lastly GH itself can bind to GH-receptors which are expressed on most cells in the body to directly stimulate growth.

67
Q

What are the 3 signalling patjways in GH-R?

A

JAK/STAT
MAPK
PI3K/AKT

68
Q

Describe how short loop negative feedback regulates the release of growth hormone?

A

GHRH is released from hypothalamus stimulates the release of GH from the somatotrophs in the anterior pituitary gland. In contrast somatostatin from the hypothalamus inhibits Gh secretion.

Circulating GH crosses the blood brain barrier to bind to GH receptors on both GHRH and somatostatin neurons in the hypothalamus.

GH through short loop negative feedback, inhibits the activity of GHRH neurons whilst stimulating GH release inhibitory neurohormone, somatostatin.

By decreasing a releasing factor GHRH and at the same time increasing a release inhibiting factor somatostatin, these together result in a decrease in GH synthesis and secretion, lowering blood GH concentrations Somatostatin acts on the anterior pituitary gland, regulating lowering GH secretion.

BIOM2011 (3 decks)

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