A study from the Diabetes, Obesity and Metabolism Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA and Division of Endocrinology and Bone Disease, Icahn School of Medicine at Mount Sinai, New York, New York, USA shows that “A high-throughput chemical screen reveals that harmine-mediated inhibition of DYRK1A increases human pancreatic beta cell replication.” This study was published in the 9 March 2015 issue of the Journal “Nature Medicine” (the no.1 journal in General Medicine with an impact factor of 28.054) by Prof Stewart AF, Wang P, and others.
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Regenerative therapy for Diabetes mellitus: ARID3B increases human pancreatic beta cell replication via down regulation of its target gene DYRK1A
Significance: Given that (1) more than 387 million people worldwide are affected by Diabetes mellitus (DM); (2) the life-long painful injection/drug treatment is required to treat DM; and (3) the global economic cost spent for diabetes treatment in 2014 was little more than 600 billion US dollars, there is an urgent need to find a way to induce regeneration of adult β-cells that were lost in DM. This study suggests, for the first time, that ARID3B, by decreasing the expression of its target gene DYRK1A, it may increase/improve: (1) human pancreatic beta cell replication; (2) islet cell mass; and (3) glycemic control. Thus, pharmacological formulations encompassing “ARID3B activators” may be used to regenerate human adult beta cells.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
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To cite: Boominathan, Regenerative therapy for Diabetes mellitus: ARID3B increases human pancreatic beta cell replication via down regulation of its target gene DYRK1A, 15/April/2015, 11.38 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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Undisclosed information: How ARID3B decreases the expression of DYRK1