There have been several trials with niacinamide on type I diabetes and it seems effective in about 40% of the cases, especially when the beta cells of the pancreas are still viable. Probably as a result of these successful studies, big pharma has been looking to capitalize on these results for the last 30 years. Using a substance that can be thought of a cousin to niacinamide, this study showed reversal of type I diabetes in mice. Of course, the scientists immediately patented the molecules but they are both aminopyrazines. Niacinamide and pyridoxal are pyridines, and thiamine is a pyrimidine.
The human equivalent dose was 3.5mg/kg and duration was only 9 days.
http://www.nature.com/ncomms/2015/15102 ... s9372.html
"...Insufficient pancreatic β-cell mass or function results in diabetes mellitus. While significant progress has been made in regulating insulin secretion from β-cells in diabetic patients, no pharmacological agents have been described that increase β-cell replication in humans. Here we report aminopyrazine compounds that stimulate robust β-cell proliferation in adult primary islets, most likely as a result of combined inhibition of DYRK1A and GSK3B. Aminopyrazine-treated human islets retain functionality in vitro and after transplantation into diabetic mice. Oral dosing of these compounds in diabetic mice induces β-cell proliferation, increases β-cell mass and insulin content, and improves glycaemic control. Biochemical, genetic and cell biology data point to Dyrk1a as the key molecular target. This study supports the feasibility of treating diabetes with an oral therapy to restore β-cell mass, and highlights a tractable pathway for future drug discovery efforts."
The human equivalent dose was 3.5mg/kg and duration was only 9 days.
http://www.nature.com/ncomms/2015/15102 ... s9372.html
"...Insufficient pancreatic β-cell mass or function results in diabetes mellitus. While significant progress has been made in regulating insulin secretion from β-cells in diabetic patients, no pharmacological agents have been described that increase β-cell replication in humans. Here we report aminopyrazine compounds that stimulate robust β-cell proliferation in adult primary islets, most likely as a result of combined inhibition of DYRK1A and GSK3B. Aminopyrazine-treated human islets retain functionality in vitro and after transplantation into diabetic mice. Oral dosing of these compounds in diabetic mice induces β-cell proliferation, increases β-cell mass and insulin content, and improves glycaemic control. Biochemical, genetic and cell biology data point to Dyrk1a as the key molecular target. This study supports the feasibility of treating diabetes with an oral therapy to restore β-cell mass, and highlights a tractable pathway for future drug discovery efforts."