Interleukin-based therapy for diabetes: IL-22 increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state, via up-regulation of  its target gene Lin28, 26/January/2019, 11.26 pm

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 IntroductionWhat 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 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 GBMDreports that:  Interleukin-based therapy for diabetes: IL-22 increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state, via up-regulation of  its target gene Lin28


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 provides, for the first time, mechanistic insight into how Runx2/AML1 may aid in the treatment of diabetes. Runx2/AML1, by increasing the expression of its target gene, it 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).

 

Figure 1. Mechanistic insights into how Runx2/AML1  functions as an anti-diabetic and a cardioprotective agent. Runx2/AML1  may promote insulin sensitivity and protect against myocardial infarction via up regulation of reprogramming protein Lin-28

Figure 2. IL-22 functions as an anti-diabetic agent through induction of Lin-28

Thus, pharmacological formulations encompassing “IL-22  or its inducers, either alone or in combination with other drugs,” may be used to treat DM and DCM.

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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 IL-22  promote insulin-sensitized state?

# Research cooperation


References

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

CitationBoominathan L, Interleukin-based therapy for diabetes: IL-22 increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state, via up-regulation of  its target gene Lin28, 26/January/2019, 11.26 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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