A study from the Department of Cancer Biology, Dana-Farber Cancer Institute; Department of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA; and others shows that “Cyclin D1–Cdk4 controls glucose metabolism independently of cell cycle progression.”
This study was published in the June 26, 2014 Nature [I.F >42] by Prof. Puigserver and others from the Department of Cancer Biology, Dana-Farber Cancer Institute; Department of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA.
On the foundation of this interesting finding, Dr L Boominathan, Director-cum-chief Scientist of GBMD, reports here that: Molecular therapy for T2DM: β-catenin inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1. This study may suggest that β-catenin, by up regulating its target gene, it may inhibit gluconeogenesis and hyperglycemia. Together, this study suggests that pharmacological formulations encompassing “β-catenin activators” can be used in the treatment of NIDDM.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
Web: http://genomediscovery.org
Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/
To cite: Boominathan, L., Molecular therapy for DM: β-catenin promotes gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, 11/February/2014, 23.19, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
Courtesy: When you cite drop us a line at info@genomediscovery.org
* Research cooperation