Let’s now move on to growth hormone.
Growth hormone, a couple of things here.
The way that this is setup is the following.
We’ll begin with the hypothalamus with our
releasing hormone/inhibiting hormone.
We’ll move from the hypothalamus into the
This is then known as your somatotroph.
Collectively, remember that growth hormone
LH share a common precursor known as somatommamotropin
and growth hormone will be released from the
anterior pituitary, works upon the liver where
it then releases your insulin-like growth
On your left, you’ll notice the following.
Remember that growth hormone is something
that’s released more so at night when one
So, therefore, that pulsatile nature making
growth hormone measurement not the most reliable
and also, the growth hormone is a stress hormone.
With that said, please look at the stimuli
on your left.
We have sleep… big time; exercise… when
you exercise, you’re consuming glucose.
Hypoglycaemia, amino acids… all of these
will be triggers for the hypothalamus to release
growth hormone releasing hormone.
On the other side of things, we have growth
hormone inhibiting hormone.
Please take a look at the key over to your
far right and you’ll notice somatostatin.
Once again I reiterate that growth hormone
inhibiting hormone is also called somatostatin.
Used to be called, once upon a time, just
to make sure we cover all basis, that insulin-like
growth factor was called somatomedin.
So, there are lot of terms here that have
the prefix somato-, somato-, somato-… somatostatin,
somtatotroph, somatomedin… mediating your
Next ,we are going to travel through our portal
By that, we mean what?
From the hypothalamus through this stalk,
through portal vein and we’re entering the
Within the anterior pituitary, what is the
name of the cell and what stain is it that
releases growth hormone?
The name of the cell is somatotroph, it stains
pink or acidophil.
It’s responsible for releasing growth hormone.
This will then work upon the liver.
From the liver, we release our insulin-like
growth factor and this insulin-like growth
factor is going to be responsible for the
vast, vast functioning of our growth hormone
including during a child when we’re growing
up into puberty, our linear growth of our
Keep in mind that the inhibitory or the feedback
mechanism for IGF1 which is the most important
measurement laboratory wise of how well our
growth hormone is functioning in our body
has a stimulatory effect on your somatostatin.
Secretion of growth hormone by somatotroph
is regulated by… we talked about growth
hormone releasing hormone and somatostatin
a.k.a. growth hormone inhibiting hormone.
If excessive growth hormone is being secreted,
then as a child, we or the child becomes a
giant or gigantism as an adult.
And if it’s an adult that has excess growth
hormone, obviously referred to as your acromegaly.
Here, we have excess amounts of somatomedins
are formed by growth hormone coming from the
It’s important that you know that somatomedin
exhibits or exerts its inhibitory effect on
your growth hormone by stimulating somatostatin.
Negative feedback signals are overridden during
sleep when growth hormone levels are highest.
That is important for you to take out of this
Hence, the pulsatile nature and the fact that
growth hormone has a shorter half-life than
IGF1 making it a less reliable laboratory
The target organ is the following.
Let me set this up… of the growth hormone
The combination of the two or each separately
has different effects, as we shall see.
Target hypothalamus releasing your growth
hormone releasing hormone works in the anterior
pituitary releasing growth hormone, out comes
the growth hormone.
The growth hormone has a couple of things.
Remember, this is stress hormone.
So, therefore, you are then going to breakdown
your lipid… lipolysis hence releasing your
free fatty acids.
You are also going to release your ketones
from your muscle, you’re going to release
Remember what are we doing here?
We are making sure that we do everything in
our power to take those cells that are going
to give us the precursors for gluconeogenesis
biochemically, aren’t we, and for protein
So, it’s going to take all of this from
our adipocytes, our liver and muscle and then
place it into circulation, hence the green
tube that you see here.
The green tube represents the circulation
and from the circulation, you’ll notice
here the somatomedin means what?
Insulin-like growth factor, coming from where?
The liver, is then responsible for growth.
It’s responsible for linear growth of your
long bones, as you see here; it’s responsible
for protein synthesis, as you can see here;
and to build everything up of your viscera.
Everything is growing and this is mostly due
to the effect of IGF1, insulin-like growth
Here, it’s showing you growth hormone working
up upon your adipocytes resulting in lipolysis.
Here, from the liver growth hormone works
through gluconeogenesis being the biochemical
Growth hormone from the liver is going to
release insulin-like growth factor 1.
From the muscle, remember, it wants to have
or bring in those amino acids, it’s the
precursor uptake protein synthesis by growth
hormone and IGF.
Here, through the action of IGF, you will
have linear bone growth, you’ll have protein
synthesis and you have a visceral maturity.
All of these would be through the actions
Prior to all these was the effect of growth
hormone on different cells and tissues…
adipocytes, muscles cells and liver.
Somatomedin, bone growth, on your viscera…
Without any of this, we have the following
In the middle, we have a normal child at the
age of approximately 13.
On your left is a patient who doesn’t have
growth hormone and this is what’s called
as Lorain levi.
On your right, you also find a suboptimal
patient with a growth hormone and this is
called Frohlich’s dwarf.
Of all the three patients and of the two that
have growth hormone dysfunction, you’ll
notice that Lorain levi are those patients
that seem to be the or have the shortest defect
or the shortest growth.
So, what’s happening here with Lorain levi?
It’s the fact that there’s an actual problem
within your growth hormone receptor.
If the receptors do not ever function, then
what do you know about the precursor hormone
or the hormone prior?
It’s always elevated.
Deficiency or absence of somatotroph cells,
underproduction of growth hormone, delayed
skeletal growth and retarded sexual development,
but alert, intelligent, well proportional
IQ perfectly okay, however as far as growth
is concerned, it is completely retarded.
Now, when you have Frohlich… in Frohlich,
the problem is the following.
A destructive disease of part of the anterior
pituitary and usually with damage to posterior
pituitary as well and that usually will help
you a little bit more.
There’s going to be decreased production
of growth hormone and because the anterior
pituitary might be affected during development;
if the thyroid hormones have been affected,
there’s going to be the most important statement
here apart from the fact that there’s going
to be stunting of growth and mental-mental
sub-normal or sub-optimal mental activity.
We did not see this with Lorain levi type
of growth hormone dysfunction.
Obesity and large appetite for sugar; if atrophy
of other endocrine glands, signs of deficiency
of their hormone.
So, with Frohlich, you’re thinking about
your anti-pituitary being more of an issue;
with Lorain levi, you’re thinking more about
your growth hormone receptor being an issue.
Know growth hormone in great detail.
What if it was growth hormone excess?
As a kid, there’s gigantism, pretty straight-forward…
long bones over grow as epiphyseal plates
are yet diffused.
As an adult, known as acromegaly, there might
be soft tissue growth, there will be visceromegaly.
There might be prognathism, the jaw that I
talked about being extremely pronounced and
increased cardiovascular mortality with reduced
life expectancy in non-cured individuals.
Because there’s visceromegaly as well, “Hey
doc, my hat size is increasing.”
Now, with that said, that gives you a couple
differentials, I’ll just name a few.
Sure, it could be acromegaly, it could also
be Paget’s disease of the bone or it could
be something like osteopetrosis.
Okay, so, the three major complaints or-or
the expression of hat size increasing once
again would be acromegaly and Paget’s disease
of the bone.
Those are the two big ones, then we’ll get
into orthopaedics, we’ll talk about Paget’s
disease of the bone further so that you clearly
distinguish acromegaly from this and the other
one technically that might also have increased
hat size includes osteopetrosis.