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 DM: CD28 promotes gluconeogenesis and hyperglycemia via up regulation of Cyclin D1. This study may suggest that CD28, by up regulating its target gene, it may inhibit gluconeogenesis and hyperglycemia. Together, this study suggests that pharmacological formulations encompassing “CD28 activators” can be used in the treatment of NIDDM.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
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To cite: Boominathan, L., Molecular therapy for DM: CD28 promotes gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, 17/September/2014, 05.48 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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