Molecular therapy for Diabetes mellitus: Unacylated ghrelin (UnAG) increases islet insulin levels, islet cell mass and glucose tolerance via down regulation of NMDA receptor GluN2A, 14/September/2016, 5.42 pm

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Idea Proposed/Formulated byDr L Boominathan Ph.D.

Undisclosed information: How Unacylated ghrelin (UnAG) decreases the expression of NMDA receptor GluN2A


A study from the Institute of Metabolic Physiology, Heinrich Heine University, Düsseldorf, Germany shows that: “Characterization of pancreatic NMDA receptors as possible drug targets for diabetes treatment.” This study was published in the 16 March 2015  issue of the Journal “Nature Medicine” (one of the best journal in “General Medicine” with an impact factor of 28) by Prof. Lammert E, Marquard J and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for Diabetes mellitus: Unacylated ghrelin (UnAG) increases islet insulin levels, islet cell mass and glucose tolerance via down regulation of NMDA receptor GluN2A

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; (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: (i) a way to induce regeneration of adult β-cells that were lost in DM; (ii) a cheaper alternative to the existing expensive weight-loss drugs; (iii) a side-effect-free natural product-based drug; and (iv) a way to cure, not just treat, diabetes.

Prof. Lammert ’s research team has showed that NMDAR antagonist dextromethorphan promotes glucose tolerance, suggesting that inhibition of NMDAR activity may  promote glucose tolerance.

This study suggests an miRNA-based therapy for diabetes mellitus.

miR-126, by decreasing the expression of its target gene, it may: (1) decrease the expression of one of the subunits of NMDA receptor, GluN2A; (2) increase islet insulin levels; (3) increase islet cell mass; and (4) improve glucose tolerance. Thus, pharmacological formulations encompassing miR-126 or its activators may be used in the treatment of T2DM.

* Research cooperation


To citeBoominathan, L., Molecular therapy for Diabetes mellitus: Unacylated ghrelin (UnAG) increases islet insulin levels, islet cell mass and glucose tolerance via down regulation of NMDA receptor GluN2A, 14/September/2016, 5.42 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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