Locking blood sugar disease with an interleukin therapy: Interleukin(IL-15)-based therapy for TIIDM: IL-15 increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state, via up-regulation of  its target gene Lin28, 1/May/2018, 10.33 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 George Q, the present Dean of the Harvard Medical School, 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: Locking blood sugar disease with an interleukin therapy: Interleukin(IL-15)-based therapy for TIIDM: IL-15 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 suggests, for the first time, that Interleukin-15, by increasing the expression of its target gene, it may increase the expression of Lin-28. Thereby, 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).

Thus, pharmacological formulations encompassing ” Interleukin-15 or its activators, either alone or in combination with other drugs,” may be used to treat DM and DCM.

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Figure 1. Mechanistic insights into how  Interleukin-15 functions as an anti-diabetic and  cardioprotective agent.  Interleukin-15  may promote insulin sensitivity and protect against myocardial infarction via up regulation of reprogramming protein Lin-28

Figure 2. The chemical structure of Interleukin-15 .  Interleukin-15  may function as an anti-hyperglycemic agent through induction of Lin-28

 

 


Details of the research findings: 

Idea Proposed/Formulated (with experimental evidence) by:

Dr L Boominathan Ph.D.

Amount: $ 500#

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

Undisclosed mechanistic information: How does  Interleukin-15 promote insulin-sensitized state?

# Research cooperation


References

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

CitationBoominathan L, Locking blood sugar disease with an interleukin therapy: Interleukin(IL-15)-based therapy for TIIDM: IL-15 increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state, via up-regulation of  its target gene Lin28, 1/May/2018, 10.34 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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