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: An unknown mechanistic insight into how analgesics normalize glucose levels: Paracetamol (4-Hydroxyacetanilide) inhibits gluconeogenesis and hyperglycemia via up regulation of its target gene CyclinD1. Paracetamol, by down regulating the expression of its target gene, it may increase the expression of CyclinD1. Thus, pharmacological formulations encompassing “Paracetamol or its analogues (free of side effects)” in non-lethal doses 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., An unknown mechanistic insight into how analgesics normalize glucose levels: Paracetamol (4-Hydroxyacetanilide) inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, 24/February/2015, 13.49, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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* Research cooperation
Undisclosed information: How Paracetamol (4-Hydroxyacetanilide) inhibits gluconeogenesis and hyperglycemia
Amount: $300*
