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My name is Marc Donath.
I'm an endocrinologist at the
University Hospital in Basel,
doing research and
working in the clinic.
My focus is on inflammation in
patients with Type 2 Diabetes.
This is the topic of today,
focusing on inflammation in the pathophysiology and
therapy of Type 2 Diabetes and associated disease.
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What we described 20 years ago
is that glucose induces IL-1β.
We described that first in
an animal model of diabetes,
Psammomys obesus,
which we put on a
high energy diet.
By doing so, IL-1β
was increased.
But then we treated the
animal with phlorizin,
which is an SGLT inhibitor.
Just by doing so,
IL-1β decreased.
This proves, in vivo, that
glucose induces IL-1β,
and that one of the mechanisms
of this SGLT2 inhibitor,
which are drugs that
induce glucosuria,
meaning that the glucose
goes into the urine,
could be that it decreases
the inflammation.
But what is important
with this talk
is to realize this principle that glucose
or metabolic stress can induce IL-1β.
We come back to this concept,
which is a general concept,
in the context of what we
call immunometabolism.
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Beyond this cytokine,
we went on to observe that in the islet
of patients with Type 2 Diabetes,
there is a real inflammation.
Not just a few cytokines,
but also immune cells,
as you can see here on the
right side of my presentation.
We had some difficulty in
having these concepts accepted,
that is that there is an inflammation in
islets of patients with Type 2 Diabetes.
We made a lot of effort in this original
publication to bring convincing data
and fortunately, in the meantime, many
others have confirmed these data.
