Ribonucleic acid-based therapy for diabetes: LncRNA UCA1  increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state, via up-regulation of  its target gene Lin28, 22/February/2019, 9.32 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: Ribonucleic acid-based therapy for diabetes: LncRNA UCA1  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 the 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 LncRNA UCA1 may aid in the treatment of diabetes. LncRNA UCA1, 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 LncRNA UCA1 functions as an anti-diabetic and a cardioprotective agent. LncRNA UCA1  may promote insulin sensitivity and protect against myocardial infarction via up-regulation of reprogramming protein Lin-28

Figure 2. LncRNA UCA1 functions as an anti-diabetic agent through induction of Lin-28

Thus, pharmacological formulations encompassing “LncRNA UCA1  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 LncRNA UCA1 promote insulin-sensitized state?

# Research cooperation


References

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

CitationBoominathan L, Ribonucleic acid-based therapy for diabetes: LncRNA UCA1  increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state, via up-regulation of  its target gene Lin28, 22/February/2019, 9.32 pm,  Genome-2-BioMedicine Discovery center (GBMD), http://genomediscovery.org

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