Let’s talk about type II.
The type II diabetes, the basic characteristics,
epidemiology: usually later in life, greater
These patients will be obese as far as you’re
concerned and a major, major genetic family
In fact, if your mother and father have diabetes,
you have close to 100 percent penetrance of
you yourself developing diabetes.
So, therefore, with that type of history,
which you as a clinician would be maybe perhaps
interviewing me, would then want to always
check for pre-diabetes, right, impaired glucose
tolerance, so on and so forth.
Here, the patho-physio that you want to know
for sure, priority would be the fact that
the insulin receptors are resistant.
Do you remember those insulin receptors with
two beta sub-units, with autophosphorylation
in tyrosine kinase?
Somewhere in that apparatus of the membrane,
the insulin receptor isn’t working.
Where’s my glucose?
Decreased peripheral glucose uptake resulting
The beta cell dysfunction is quite interesting,
we’ll walk you through this.
So, initially, the patient becomes obese.
Okay, gradually; you don’t become obese
As it goes on to become obese, the insulin
receptors are working less and less and less
which means that now the patient is increasing
their glucose step by step by step overtime.
In type II diabetes, it’s still possible
that you have insulin in your pancreas, correct?
Yes, therefore, with that hyperglycemia early
on, do you think that your patient with type
II diabetes might have hyperinsulinemia?
Yeah, lot of research mind you with this because
that hyperinsulinemia can actually wreak havoc
up and down the body.
For example, take a look at the armpits of
a patient with type II diabetes or the back
of the neck of type II diabetes and you’ll
notice there’s darkening of the skin.
Nigra means dark; acanthosis means thickening…
thickening of the keratinocytes, therefore
giving you the presentation of dark skin underneath
the armpits and maybe the back of the neck.
Maybe the insulin in fact, there’s a lot
of evidence out there that that increased
insulin early on in type II diabetes may then
Perhaps even the atherosclerosis, maybe even
Insulin level increased… now, you understand
If you do not follow my discussion just now,
this becomes rather difficult.
Early on, you can have increased levels of
insulin, but at some point in time what happens?
Well, with the pancreas, you might exhaust
all levels of insulin.
What’s your first step of management?
Discipline, lifestyle modification, exercise,
watch your diet.
If that doesn’t work, patient’s non-compliant,
then you start thinking about oral hypoglycemic
Worst case scenario… insulin.
Complications… ketoacidosis is rare, but
can occur after stress such as surgery…
type II diabetes.
Pathology, couple of important things here.
Fibrosis and hyalinization… fibrosis and
Fibrosis might be found in the pancreas, you
can have an amyloid and we’ll talk about
it in a little bit called amylin and if you’re
thinking about type II diabetes and you’re
referring to what’s known as arteriolosclerosis…
arteriolosclerosis, there are two kinds remember?
You’re putting things together?
Hyaline, arteriolosclerosis; hyperplastic,
Which one is it that you find in type II diabetes
Non-conventional type II diabetes… similar
to type II, occurs in the young.
Increasing in frequency, meaning to say as
we gain better understanding of diabetes mellitus,
we actually find this as being increasing
type of diagnosis, genetically inherited,
this is important.
It’s one thing that you want to take out
of the symptoms referred to as being MODY.
MODY, stands for Maturity Onset of Diabetes
in the Young, M-O-D-Y.
Usually genetic proponent, may usually develop
type II diabetes.
So, therefore, do not confuse this with type
Type I diabetes, young patient, maybe about
24, 25; MODY maturity onset of diabetes in
the young… young patient, maybe 24, 25.
Type I diabetic, insulin is not going to be
You’re worried about hyperglycemia.
The only method of treatment would be to give
Here, however, glucokinase could be a problem.
One of the first enzymes in the glycolytic
pathway… not the rate-limiting enzyme, but
the first stanza.
So, if glucokinase is not present, then what
May result in hyperglycemia not conventional
and may then go on to develop type II diabetes.
This is not present at all in type I.
Could be insulin molecule issues, insulin
receptor or perhaps even glucose transporter
4, but the big one that you want to take out
of this is the first bullet point of glucokinase…