Increasing beta cells in persons who have one of the High Glucose Conditions?
- From: "Pro-Humanist FREELOVER" <prohuman@xxxxxxxxxxxx>
- Date: Wed, 20 Jun 2012 07:02:49 -0500
- - -
Precautionary note -- Mice Research,
unclear if or when this might be tested
in humans, and unclear what would
have to occur in order for something
like this, in altered form, to be of use
in dealing with High Glucose Conditions
In the following article, the term "dia-
betes" is used 4 times without clarifier.
In that the effort increased beta cells
in mice, and autoimmunity was not
addressed, it appears that the type of
treatment would (some day, perhaps)
be of benefit in preventing or placing
the condition of Cellosis (old name:
type 2 diabetes) into remission.
However, this ability would not (with-
out some way to turn off the auto-
immune attack which causes Insulinitis,
old name: type 1 diabetes, in the over-
whelming majority of cases) be able to
prevent that autoimmune attack from
continuing in those who have Insulinitis.
Also, those who have Insulinitis due to
their pancreas suffering removal or
severe dysfunction due to other condi-
tions, this treatment, difficult to con-
ceive of a way that it could actualize
Diminosis (old name: Mature Onset
Diabetes of the Young), this might be
able to prevent or place that condition
into remission, some day.
Also, this treatment, if a way was found
to turn off the autoimmune attack which
causes Insulinitis in the overwhelming
majority of cases, if combined with that,
could cure Insulinitis, in those whose
Insulinitis was not caused by the removal
of their pancreas, some day.
However, caution is advised, as this was
discovered as a sidenote to research that
wasn't trying to find treatments or cures
for any High Glucose Condition, and it
would require substantial further work
prior to even approaching testability in
- - -
June 20, 2012
Gene deactivation can fight ...
[High Glucose Conditions; see above for
the actual nature of the treatment dis-
cussed in the following, and note that
this treatment does not address the
overwhelming causality of Insulinitis,
that being an autoimmune attack on
pancreatic beta cells, which would have
to be addressed in order for the treat-
ment to actualize insulin production
without it being destroyed in a contin-
ued autoimmune attack in those who
In a major breakthrough that could help
in fighting [High Glucose Conditions, with
exceptions noted above], a team of re-
searchers from the city-based Centre for
Cellular and Molecular Biology has success-
fully deactivated a gene to regulate the
functioning of beta cells in pancreas.
The research team ... created a mouse
model without the presence of the gene,
Wdr13 (WD-repeat protein), using genetic
engineering technology. The team inacti-
vated or knocked out the gene by disrupt-
ing it through insertion of an artificial piece
of DNA in the embryonic stem cells.
The removal or inactivation of the gene
WDr13 in mouse model led to formation
of more pancreatic mass in the islets of
Langerhans. This showed that the knock-
ing of the gene would lead to formation
of more beta cell mass in pancreas. The
mouse showed higher levels of insulin in
blood serum, and thus better ... blood
According to the Centre for Cellular and
Molecular Biology team, the protein could
be helpful in finding a potential drug tar-
get to treat [Cellosis and Diminosis, but
dealing with Insulinitis would continue to
be problematic] ...
- - - - - - - - - - - - - - - -
- - -
June 20, 2012
Finding holds potential for drug targeting
to treat ... [High Glucose Conditions, with
exceptions noted above]
Scientists from the Centre for Cellular and
Molecular Biology (CCMB) have found that
knocking out a gene in mice led to higher
insulin production and better glucose toler-
ance. The finding holds the potential for
drug targeting to treat ... [High Glucose
Conditions, with exceptions noted above].
The team, led by Satish Kumar, serendipi-
tously found that knocking out the WDR13
gene, resulted in hyper insulin secretion
and improved glucose clearance. The team
genetically engineered a mouse by knocking
out the gene, which is conserved in all organ-
isms from fishes to humans and encodes a
protein. It is a member of the WD-repeat
proteins that have a wide range of cellular
The increase in insulin production was caused
by enhanced beta cell proliferation and higher
islet mass in pancreas.
The test animals went on to develop mild
obesity as they aged. Interestingly, however,
they continued to have better glucose clear-
ance in spite of mild obesity. It was not yet
known if the obesity was due to higher insulin
levels or some different function of the gene.
Dr. Kumar told The Hindu that by inhibiting
the functions of this protein, insulin production
could be enhanced.
?Indirectly, we discovered a drug target be-
cause now we know that if we interfere with
this protein, there is more insulin,? he said.
However, he noted that there was a flipside
to the finding. While there was no problem
with the ?knockout' mice up to one year, sub-
sequently, their cell proliferation increased
? such phenomenon lead to tumours.
The researchers were not aware of the
WDR13's function of regulating cell division.
The real challenge would be to develop a
drug, which would interfere in a limited way
with the functioning of the gene, so as to
avoid rapid cell proliferation.
Dr. Kumar said their research initially was
not related to ... [High Glucose Conditions].
?We were doing basic biology. This is side
implication with an interesting lead.?
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C.ure I.nsulinitis A.ssociation
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