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Diabetes "Cured" In Mice With Virus Therapy
phlack writes "Scientists at Baylor College of Medicine have found a way to treat diabetes in mice by using a virus (with the harmful genes removed) to trick the liver into working as a pancreas. This is still a ways away from working in humans, but it's progress, at least. Info can be found at Guardian and Science Daily."
All the need to do is invent another virus that makes some other organ function as a liver!
I've had enough abrasive sigs. Kittens are cute and fuzzy.
I have to wonder what takes the place of the liver. (Articles have been
Given the choice between a normal liver plus insulin injections, versus a "virtual pancreas" and some unknown liver treatment, I think I'd stick with the devil I knew.
More precisely, I know how my body reacts to insulin injections. Nobody knows how it would react to - ah screw it, I can't seem to express this thought coherently.
You cannot apply a technological solution to a sociological problem. (Edwards' Law)
FYI - The real question about this, and other gene therapy experiments, focueses on the safety of the vector being used. In this case an adenovirus virus was used. The virus itself is no longer virulent, but how does the target genetic material get integrated into the hosts genome? If it occurs at a specific site, then safety is maximized. If it occurs randomly, then you run the risk of knocking out genes where only a single healthy allele exists (loss of heterozygosity) and potentially, cancer.
Gene therapy holds a lot of promise, but the early cases of leukemia (remember the bubble boy cure? Two 'cured' patients subsequently developed cancer) make it prohibative. I'm an expert enough to know this a problem (in theory and in practice) but not enough of one to know how close we are to solving it.
-Sean
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I just read the Nature Medicine article and the authors speculate that they were able to induce differentiation of hepatic stem cells or hepatocytes into islet-like cells, and it looks very convincing. A potential major shortcoming of this approach is not addressed, which is that in type I ("juvenile") diabetes, the islet cells are destroyed by an autoimmune response. Thus if you generate new self "pseudo islets", you may have present the very antigens that led to their destruction in the first place. The reason that is not a problem in this experiment is that the authors artificially destroy the islets with the toxin streptozotocin. The real test would be in an animal model that mimics type I diabetes, like the non-obese diabetic (NOD) mouse. I hope and assume that is the next critical experiment.
Up to 2/3 of your liver may be destroyed (or poisoned) and it will still function correctly. I very much doubt that anything like this much will be affected by this process. Therefore it is safe to assume that there will be no percieved effects of this treatment other than the positive!
This sort of advance should work very well for people who have type I diabetes, where their bodies no long secrete insulin. I have to wonder how well it will work in people with adult-onset, type II diabetes, which is triggered by a malformed receptor that isn't sensitive enough to secreted insulin. The use of oral or injectable insulin might be eliminate, but I worry that the attendant physical ailments, such as diabetic retinopathy, will still dog those who suffer. Unfortunately, the problem of fixing those receptors may prove to be much more difficult.
C'mon, fellas... CBC's science program Quirks & Quarks
reported (over 18 months ago) that islet transplants
were suceeding in almost 90% of cases.
A further development (by a private sector co.)
reported greater success rates or fewer problems.
Let's get this story as well, eh?