From: Alan Mackenzie on
[Translation of an article by Anja Lange in de.sci.medizin.diabetes.
Thanks, Anja!]

<http://www.medicalnewstoday.com/articles/110813.php> describes a study in
which two new drugs were combined in order to reverse the effects of T1
diabetes. ("Effects" here means the damage to the pancreas, not any
associated complications.)

The first drug acts as a brake on the damage that the immune system does to
the beta cells and the second encourages the formation of new insulin
producing beta cells.

It has become clear that the body has an innate ability to repair and
regenerate beta cells, in contrast to the previous assumption that their
destruction was irreversible, just that it can't keep up with the response of
the immune system. Researchers are thus trying this drug combination to
accelerate the slow rate of regeneration and slow the response of the immune
system.

Mice rendered diabetic for this study received either a placebo, just one of
the drugs, or both together. There was a clear remission rate and a pretty
much normal serum insulin concentration [?in the double-drugged mice].

See the report at <http://www.medicalnewstoday.com/articles/110813.php>.

--
Alan Mackenzie (Nuremberg, Germany).

From: W. Baker on
Alan Mackenzie <acm(a)colin2.muc.de> wrote:
: [Translation of an article by Anja Lange in de.sci.medizin.diabetes.
: Thanks, Anja!]

: <http://www.medicalnewstoday.com/articles/110813.php> describes a study in
: which two new drugs were combined in order to reverse the effects of T1
: diabetes. ("Effects" here means the damage to the pancreas, not any
: associated complications.)

: The first drug acts as a brake on the damage that the immune system does to
: the beta cells and the second encourages the formation of new insulin
: producing beta cells.

: It has become clear that the body has an innate ability to repair and
: regenerate beta cells, in contrast to the previous assumption that their
: destruction was irreversible, just that it can't keep up with the response of
: the immune system. Researchers are thus trying this drug combination to
: accelerate the slow rate of regeneration and slow the response of the immune
: system.

: Mice rendered diabetic for this study received either a placebo, just one of
: the drugs, or both together. There was a clear remission rate and a pretty
: much normal serum insulin concentration [?in the double-drugged mice].

: See the report at <http://www.medicalnewstoday.com/articles/110813.php>.

: --
: Alan Mackenzie (Nuremberg, Germany).

I can understand how a mouse could be rendered diabetic by doing something
to its pancras, but can you make a mouse type 1 with an immune system tht
keeps on destroying any beta cells produced? I can also understand
breeding mice with a strong tendancy to be type 1, but not how to change
oone into a tye 1.

Wendy
From: Alan Mackenzie on
Hi, Wendy!

W. Baker <wbaker(a)panix.com> wrote:
> Alan Mackenzie <acm(a)colin2.muc.de> wrote:

[ .... ]

> : Mice rendered diabetic for this study received either a placebo, just one of
> : the drugs, or both together. There was a clear remission rate and a pretty
> : much normal serum insulin concentration [?in the double-drugged mice].

[ .... ]

> I can understand how a mouse could be rendered diabetic by doing something
> to its pancras, but can you make a mouse type 1 with an immune system tht
> keeps on destroying any beta cells produced? I can also understand
> breeding mice with a strong tendancy to be type 1, but not how to change
> oone into a tye 1.

I don't know. Quite honestly, I don't want to find out, either. ;-)
Alternatively, I might have misunderstood the original German. I'm glad
I'm not one of these mice, though.

> Wendy

--
Alan Mackenzie (Nuremberg, Germany).

From: Charly Coughran on
"W. Baker" <wbaker(a)panix.com> wrote in
news:g4rmdr$afd$1(a)reader1.panix.com:

>
> I can understand how a mouse could be rendered diabetic by doing
> something to its pancras, but can you make a mouse type 1 with an
> immune system tht keeps on destroying any beta cells produced? I
> can also understand breeding mice with a strong tendancy to be type
> 1, but not how to change oone into a tye 1.
>
> Wendy

You do it by breeding. The NOD mouse, one of several mouse models of
type 1, is genetically bred to have a high incidence of autoimmune beta
cell destruction. 80-90% of females and 20-50% of males will
spontaneously develop autoimmune caused diabetes between age 3-6 months.
--
-------
Charly Coughran
ccoughran(a)DELETE-TO-RESPOND-UCSD.EDU
From: Charly Coughran on
Wes Groleau <groleau+news(a)freeshell.org> wrote in
news:2Jwck.713$713.272(a)trnddc03:

> Alan Mackenzie wrote:
>> [Translation ....]
>>
>> The first drug acts as a brake on the damage that the immune system
>> does to the beta cells and the second encourages the formation of
>> new insulin producing beta cells.
>
> If its true that Type 2s typically have significant beta cell loss,
> I wonder whether the second drug might be worthwhile for us.
>

The beta cell loss, which is common in type 2 diabetics, is not
autoimmune. The genetics responsible for that loss are complex and not
well understood except in a few monogenic (single gene) syndromes.

--
-------
Charly Coughran
ccoughran(a)DELETE-TO-RESPOND-UCSD.EDU