Small molecule based-therapy for Regenerating the lost pancreatic β-cells in Diabetic patients: Trichostatin A, a histone deacetylase inhibitor, increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state via up-regulation of its target, 5/April/2017, 6.21 am

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Introduction: What they say

A study from the Stem Cell Transplantation Program, Division of Pediatric Hematology/Oncology, Boston Children’s Hospital and Dana-Farber Cancer Institute, Boston, Massachusetts, USA shows that “The Lin28/let-7 axis regulates glucose metabolism.” This study was published in the 30 September  2011 issue of the Journal “Cell” [One of the best journals in Biological sciences with an I.F of 28.71]  by Prof and Dean of the Harvard Medical School D George Q, Zhu H, and others.


What we say

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Small molecule based-therapy for Regenerating the lost pancreatic β-cells in Diabetic patients: Trichostatin A, a histone deacetylase inhibitor, increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state via up-regulation of  its target [easy_payment currency=”USD”]

Price 100


From significance of the study to Public health relevance

Given that: (1) more than 387 million people worldwide are affected by Diabetes mellitus (DM); (2) Diabetes is going to be one of the top 10 causes of death by 2030; (3) 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 ß-cells and cardiomyocytes that were lost in DM (Diabetes Mellitus) and MI (Myocardial infarction), respectively; (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.


What is known?

Prof. George Q and his research team members had shown earlier that loss of Lin28 in muscles promotes insulin resistance and glucose intolerance. 


From Research findings to Therapeutic opportunity:

This study suggests, for the first time, that Trichostatin A, by increasing the expression of its target geneit may (1) increase the expression of IGF1R, INSR, and IRS2; (2) enhance tissue repair; (3) promote regeneration of pancreatic β-cells; (3) augment regenerative capacity; (4) promote insulin sensitivity; and (5) protect against dilated cardiomyopathy (DCM) (Fig.1).

Trichostatin A  induces Lin28 and promotes insulin sensitivity

Figure 1. Mechanistic insights into how Trichostatin A functions as an anti-diabetic and a cardioprotective agent. Trichostatin A may promote insulin sensitivity and protect against myocardial infarction via up regulation of reprogramming protein Lin-28

Thus, pharmacological formulations encompassing “Trichostatin A or its analogues either alone or in combination with other
drugs” 
may be used to treat DM and DCM.


Details of the research findings: 

Idea Proposed/Formulated (with experimental evidence) by:

Dr L Boominathan Ph.D.

Amount: $ 100

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Undisclosed mechanistic information: How does Trichostatin A promote insulin-sensitized state?

# Research cooperation


References

Web: http://genomediscovery.org or http://newbioideas.com/

CitationBoominathan L, Small molecule basedtherapy for Regenerating the lost pancreatic β-cells in Diabetic patients: Trichostatin A, a histone deacetylase inhibitor, increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state via up-regulation of  its target, 5/April/2017, 6.21 am,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

Courtesy: When you cite drop us a line at info@genomediscovery.org

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