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Locking blood sugar disease with an interleukin therapy: Interleukin(IL-2)-based therapy for TIIDM: IL-2 increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state, via up-regulation of  its target gene Lin28, 1/June/2018, 11.23 pm

Unknown action of a known drug in body weight control, energy homeostasis and TIIDM:Bromocriptine (trade name:Parlodel), used in the treatment of  pituitary tumors, Parkinson’s disease (PD), hyperprolactinaemia, infertility and others, increases REV-ERB and its down stream target genes, inhibits lipid accumulation, improves dyslipidemia and insulin sensitivity, increases energy utilization, promotes weight loss and protects from diet-induced obesity and TIIDM, via up regulation of its target gene, 1/June/2018, 11.14 pm
June 1, 2018
Unknown action of a known drug in rescuing blood sugar disease: Bromocriptine-based adjunct therapy for autoimmune diabetes (TIDM): Bromocriptine (trade name:Parlodel), used in the treatment of  pituitary tumors, Parkinson’s disease (PD), hyperprolactinaemia, infertility and others, increases PD-L1 expression, increases Tregs function, promotes immune tolerance, increases pancreatic β-cell proliferation and regeneration, increases insulin secretion, improves insulin sensitivity, increases energy utilization, and reverses TIDM, via up regulation of its target gene, 3/June/2018, 7.32 pm
June 3, 2018
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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-2)-based therapy for TIIDM: IL-2 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-2, 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-2 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-2 functions as an anti-diabetic and  cardioprotective agent.  Interleukin-2  may promote insulin sensitivity and protect against myocardial infarction via up regulation of reprogramming protein Lin-28

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

 


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-2 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-2)-based therapy for TIIDM: IL-2 increases the expression of IGF1R, INSR, and IRS2, and promotes an insulin-sensitized state, via up-regulation of  its target gene Lin28, 1/June/2018, 11.23 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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