Molecular therapy for Regenerating the lost pancreatic β-cells in Diabetic patients: Chitooligosaccharides, one of the degradative products of Chitosan, increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state via up-regulation of its target gene, 2/April/2017, 7.49 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 SchooGeorge 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: Molecular therapy for Regenerating the lost pancreatic β-cells in Diabetic patients: Chitooligosaccharides, one of the degradative products of Chitosan,  increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state via up-regulation of  its target gene[easy_payment currency=”USD”]

Price 300


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:

Chitosan is derived from the shells of Shrimps. Chitooligosaccharide is one of the degradative products of Chitosan. 

This study suggests, for the first time, that Chitooligosaccharide, 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).

Chitooligosaccharides induce Lin28 expression and alleviate TIIDM and MI

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

Thus, pharmacological formulations encompassing Chitooligosaccharide 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: $ 300

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

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

# Research cooperation


References

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

CitationBoominathan L, Molecular therapy for Regenerating the lost pancreatic β-cells in Diabetic patients: Chitooligosaccharides, one of the degradative products of Chitosan,  increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state via up-regulation of  its target gene, 2/April/2017, 7.49 am,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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