It seems to work in mice:
Last year, Dr Terry Strom and his team demonstrated that they could stop the on-going destruction of insulin-producing beta cells in mice using a combination of three drugs, although they were unable to regenerate the cells.
However, when they added an extra ingredient – an enzyme called alpha 1 anti-trypsin – a significant rise in the number of beta cells was seen.
I’m not sure what the point is here:
It is exciting that these drugs could stop the immune system from attacking insulin-producing cells, but it is too early to tell whether these cells recovered in the mice or if new cells were produced.
Does it matter, from a practical standpoint? I can understand why the researchers would be curious, but a cure is a cure.
Anyway, here’s hoping that it can work in higher mammals.
A cure is a cure, but I suppose they would want to understand it as well as they can before they start prescribing it for human beings. I wonder what standard of theoretical understanding is required (legally and/or ethically) for a cure that demonstrably works?
I would imagine that a cell “recovered” is already there and represents a dead-end improvement, but new cells would mean that improvement could continue until full capacity returns. I’m not a doctor or biologist, though, so maybe I’m wrong.
It matters because human trials are extraordinarily expensive, not just up front, but in terms of time wasted if you do them wrong and have to do them over. If the stuff merely stops the killing of beta cells then you’ll want to focus human research on people who are not yet fully diabetic, who have some cells left to save.
That said, it’s a long way from Mus muscus to Homo sap. Don’t hold your breath for this one.