A study from the Department of Cancer Biology, Dana-Farber Cancer Institute; Department of Cell Biology, Harvard Medical School, 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 >35] by Prof. Puigserver and others from the Department of Cancer Biology, Dana-Farber Cancer Institute; Department of Cell Biology, Harvard Medical School, USA.
On the foundation of this interesting finding, Dr L Boominathan, Director-cum-chief Scientist of GBMD, reports here that: Molecular therapy for NIDDM: Pitx2 inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1.
Significance:
Given that: (1) more than 387 million people worldwide are affected by Diabetes mellitus (DM); (2) Obesity is one of the main cause for the development of T2DM; (3) the life-long drug treatment required to treat DM; and (4) 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 a way to increase insulin sensitivity in obese individuals.
This study suggests that Pitx2, by down regulating its target gene, it may inhibit gluconeogenesis and hyperglycemia. Together, this study suggests that pharmacological formulations containing “Pitx2 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 NIDDM: Pitx2 inhibits gluconeogenesis and hyperglycemia via up regulation of Cyclin D1, Genome-2-Bio-Medicine Discovery center (GBMD), 11/06/2014, 8.40 am., http://genomediscovery.org
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# Research cooperation