Good news! Possibly a breakthrough in diabetes treatment, but this is very early research! Just a few days ago, I blogged here about a breath test to monitor glucose levels.
"Australian scientists have demonstrated a new way to restore insulin production in pancreatic cells, using a drug that’s already approved for use in humans. The study could mark a major breakthrough towards new treatments for diabetes. ...
In lab experiments on pancreatic stem cells from donors with type 1 diabetes, the team was able to activate them to begin expressing insulin by exposing them to a drug compound known as GSK126. ...
The new treatment would work much faster, within a matter of days, and without the need for surgery. But perhaps the biggest advantage is that GSK126 is already approved by the US FDA and elsewhere in the world as a treatment for cancer. ..."
In lab experiments on pancreatic stem cells from donors with type 1 diabetes, the team was able to activate them to begin expressing insulin by exposing them to a drug compound known as GSK126. ...
The new treatment would work much faster, within a matter of days, and without the need for surgery. But perhaps the biggest advantage is that GSK126 is already approved by the US FDA and elsewhere in the world as a treatment for cancer. ..."
From the abstract:
"Type 1 diabetes (T1D) is an autoimmune disease that selectively destroys insulin-producing β-cells in the pancreas. An unmet need in diabetes management, current therapy is focussed on transplantation. While the reprogramming of progenitor cells into functional insulin-producing β-cells has also been proposed this remains controversial and poorly understood. The challenge is determining why default transcriptional suppression is refractory to exocrine reactivation. After the death of a 13-year-old girl with established insulin-dependent T1D, pancreatic cells were harvested in an effort to restore and understand exocrine competence. The pancreas showed classic silencing of β-cell progenitor genes with barely detectable insulin (Ins) transcript. GSK126, a highly selective inhibitor of EZH2 methyltransferase activity influenced H3K27me3 chromatin content and transcriptional control resulting in the expression of core β-cell markers and ductal progenitor genes. GSK126 also reinstated Ins gene expression despite absolute β-cell destruction. These studies show the refractory nature of chromatin characterises exocrine suppression influencing β-cell plasticity. Additional regeneration studies are warranted to determine if the approach of this n-of-1 study generalises to a broader T1D population."
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