Why is
this? Simply put, because in Type 1 cases the body's auto-immune system attacks
the pancreas. Such an attack could be due to a genetic predisposition triggered
by a virus. Whatever the case, this attack response damages the insulin
producing beta cells of the pancreas thereby leaving the pancreas no longer
able to produce the insulin required for normal blood sugar regulation. As a
result complications arise - organs of the body; eyes, kidney, heart and limbs
get affected.
The general
prognosis before now was that the condition was incurable. This belief has
however changed over time, metamorphosing into diabetes cure research focused
on the transplantation of the insulin producing cells of the pancreas destroyed
under this disease. Risks associated with the procedure however include, the
failure of the transplanted cells to function, side effects of
immune-suppressants used during the procedure and excessive bleeding or death.
Focus is
now being placed on understanding the mechanisms of the immune attack
responsible for the disease and finding ways to block it. That said though,
last year, in an apparent move towards a cure, researchers claimed to have
found a novel large-scale method enabling them to turn human embryonic stem cells
into fully functioning beta cells capable of producing insulin. They did this
by the controlled differentiation of stem cells.
Differentiation
or Cellular differentiation is the process by which a cell become specialized
in order to perform a specific function - as in the case of a blood cell,
kidney cell, heart cell, etc. Stem cells are marked out for this ability to
undergo differentiation. According to the study's co-author, Douglas Melton of
Harvard University ""We wanted to replace insulin injections using
nature's own solution, being the pancreatic beta cell... " Now "we
are reporting the ability to make hundreds of millions of these cells," he
added.
The next
step then was transplantation but they also needed to see how they could
prevent, as often happened in transplantation cases, the rejection of the
created beta cells by the body's immune system. They achieved this by creating
a device which they discovered not only protected beta cells implanted into the
test mice, but left the pancreas months after, still producing insulin.
Besides
being highly promising for type 1 diabetics, this procedure has equal potential
as treatment for many type 2 diabetics who depend on insulin injections as part
of their daily treatment regimen.
What
makes this particular breakthrough special is that unlike past successes at
deriving beta cells from stem cells, this development was able to create
glucose sensing, insulin secreting beta cells.
In focus
now, would be human trials which Melton figures could kick off in a few years'
time. Ultimately he says, the final product would be a credit card-sized
package of beta cells ensconced in an encapsulation device that would allow
sugar and insulin to easily pass through, while preventing the reverse passage
of the larger bodied immune T-cells. This package could then be safely
transplanted into a diabetes patient and left in place for a year or more
before needing replacement.
The other
method for creating beta cells which could ultimately eliminate the need for
such yearly or regular replacement would be to use pluripotent stem cells as
the base cells for differentiation rather than embryonic stem cells.
Pluripotent
stem cells are stem cells from specialized adult cells but which have been
somehow reprogrammed to change into an undifferentiated state. An example of
this is endometrial derived stem cells (hEMSCs) - cells derived from the
uterine endometrium. Research shows that these can be guided to differentiate
into insulin producing beta cells.
The newly
differentiated cells could possibly then be grafted onto the damaged pancreas
(provided the initial diabetes trigger factor is avoided), for insulin to be
produced. This would be ideal, because if one were to use a diabetics own
pluripotent stem cell as the base for beta cell cultivation, it should
eliminate the risk of the beta cells rejection. This would in turn eliminate
the need for auto-immune protective devices and in that vein interval device
replacement.
Finally,
scientists at the Harvard Stem Cell institute have identified another strategy
towards curing early stage type 1 as well as type 2 diabetes. It involves
stimulating beta cells through drug therapy to make more of themselves. Since
beta cells naturally replicate themselves, however at a slow rate, inducing them
to do so faster, would equally eliminate the need for transplantation and
immune protective devices.
As such,
with the foregoing development, it is obvious that prospects for finding a cure
for Type 1 diabetes is no longer as bleak as previously thought. In fact it is
feasible that within the decade, various methods for curing the disease would
not only be available but become essentially routine.
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