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A study from the Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan shows that “Angiopoietin-like protein 2 promotes chronic adipose tissue inflammation and obesity-related systemic insulin resistance.” This study was published in the 30 September  2009 issue of the Journal “Cell Metab.”  by Prof Oike Y, Tabata M, and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for Inflammation-mediated T2DM: Tumor suppressor p53 homologue p63 suppresses adipose tissue inflammation and insulin resistance via down regulation of Angptl2 

Significance:  This study suggests, for the first time, that  p63, by increasing the expression of its target gene, it may suppress the expression of Angiopoietin-like protein 2 (Angptl2). Thereby, it may ameliorate adipose tissue inflammation and systemic insulin resistance. Thus, pharmacological formulations encompassing “p63 activators” may be used to treat DM.

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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Undisclosed information: How p63 decreases the expression of Angiopoietin-like protein 2 (Angptl2)

To citeBoominathan, Molecular therapy for Inflammation-mediated T2DM: p63 suppresses adipose tissue inflammation and insulin resistance via down regulation of Angptl2, 4/April/2015, 08.46 am,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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