IRIG: O-GlcNAc and PGC-1 in Nature

           The negative-feedback loop in the insulin signaling pathway is a framework for the concept of post-receptor signaling defect theory, which represents the mainstream views of insulin resistance. In the school, inhibition of insulin receptor substrates (IRSs) by serine/threonine kinases is the core. Many molecular hypotheses for insulin resistance, such as inflammation, ER stress, mitochondrial dysfunction, oxidative stress, hyperinsulinemia, and hypoadiponectinemia, are built on the core. A new study in Nature enriched the theory by demonstration that insulin may promote IRS-1 inhibition by increasing glycocylation of IRS-1. The enzyme O-GlcNAc transferase (OGT) mediates this activity of insulin. This paper is recommended by Dr. Marina Bouché at the University of Rome, Italy.  (See PDF file attached).
 
            PGC-1a is another “star” molecule like SIRT1. PGC-1a is a transcription coactivator originally identified in the study of PPARg. PGC-1a is involved in glucose homeostasis, mitochondrial biogenesis, circadian rhythm, and energy expenditure. A new study in Nature shows that PGC-1a is involved in protection of microcirculation from ischemia damage by promoting angiogenesis. The mechanism is induction of VEGF expression by PGC-1a. (See PDF file attached).     
 
 
           By the way, the “Insight” section of Nature is focused on Cardiovascular disease in this issue. It contains eight excellent reviews about different aspects of CVDs. Here is the link: http://www.nature.com/nature/index.html
  
 
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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