IRIG: PGC-1/Akt interaction in "Nature" and PPARg regulator in "Cell"

08/25/2007 23:27
Liver produces glucose from amino acids through gluconeogenesis. If glucose is too much to be consumed by the peripheral tissues (muscle or fat), liver will covert the carbohydrate into fatty acids or triglycerides through hepatic de novo lipogenesis, resulting in an increase in plasma triglyceride and a reduction in plasma high-density lipoprotein. This is demonstrated in human in a new study in PNAS (See attachment 1). The hepatic gluconeogenesis and lipogenesis is regulated by insulin, which inhibits the two processes through the PI3K/Akt signaling pathway. In a “Nature” paper, a new event at downstream Akt is identified for the insulin-mediated inhibition. Akt2 was found to phosphorylate PGC-1 resulting in inhibition of PGC-1 function (See attachment 2). This event leads to shutdown of gene expression in the programs for gluconeogenesis and lipogenesis in the liver. PGC-1 is a coactivator of PPARg. In a “Cell” paper, a small molecule (Harmine) from a botanical product was found to increase insulin sensitivity by inducing PPARg gene expression. Harmine acts by inhibition of the Wnt signaling pathway (See attachment 3, 2MB in size).
 
The paper in attachment 1 is recommended by Dr. Zhenqi Liu (University of Virginia School of medicine), and paper in attachment 3 is recommended by Dr. Eugene Chen (University of Michigan Medical Center).
 
Have a nice weekend.
        
By Jianping at PBRC

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Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225)763-3163
E-mail: yej@pbrc.edu
Webpage: http://labs.pbrc.edu/generegulation/index.htm
 
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