Scientists report in the May 9 Science Translational Medicine that seven of 12
diabetic mice treated with this combination were cured even after having lost the ability to make insulin for several weeks, the equivalent of a human patient who has needed insulin injections for a couple of years.
Not exact matches
They compared the concentrations of proteins in the retinas of non-
diabetic mice, of
mice with type 2 diabetes without treatment and of type 2
diabetic mice that were
treated with the standard drug metformin, which lowers blood glucose levels and thus reduces diabetes complications.
They demonstrated that non-obese
diabetic (NOD)
mice treated with a specific (AID / RAD51) pathway inhibitor had larger populations of certain B cells that were capable of suppressing diabetogenic T cell responses, and greatly reduced T1D development, compared with untreated controls.
In these two microscopy images, human islets (the source of insulin cells) were poisoned with a drug to remove the insulin cells, and then
treated with either an empty virus (left panel) or the therapeutic virus (right panel), and then grown in a
diabetic mouse.
The blood sugar of the
diabetic mice were made normal by the gene - therapy -
treated human islets on the right.
In fact, the speed and kinetics of touching down to safe blood glucose levels are identical in
diabetic mouse models
treated with Ins - PBA - F and in healthy
mice whose blood sugar is regulated by their own insulin.
No significant difference in body weight was observed in the groups
treated with
diabetic pancreas homogenate, containing IAPP aggregates or synthetic IAPP aggregates, prepared in vitro, compared with Tg - hIAPP
mice injected with buffer (Fig. 8 A).
And,
treated,
diabetic mice had much less tissue damage compared to the untreated
diabetic mice.