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 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 GBMD, reports 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).
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.
Details of the research findings:
Idea Proposed/Formulated (with experimental evidence) by:
Dr L Boominathan Ph.D.
Amount: $ 100#
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Undisclosed mechanistic information: How does IL-22 promote insulin-sensitized state?
# Research cooperation
Citation: Boominathan 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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