Saturday, November 12, 2011
Knocking out Key Protein in Mice Boosts Insulin Sensitivity
A recent article reports on research conducted by a team of scientist at the University of California, San Diego School of Medicine and the Ecole Polytechnique Federale de Lausanne in Switzerland (EPFL). In their work with NCoR, a transcriptional coregulatory protein found in many cells, these scientists were able to reveal the positive effects the deletion of NCoR could have on insulin resistance. Increased levels of insulin sensitivity were observed in the liver, muscle, and fat of mice that had NCoR knocked out; a decrease in systemic inflammation was also observed. In addition to this, the deletion of NCoR in adipocytes also accompanied an increase in PPAR-gamma or Peroxisome Proliferator-Activated Receptor gamma, a protein that regulates fatty acid storage and glucose metabolism: increased PPAR-gamma furthered insulin sensitivity. EPFL scientists discovered that knocking NCoR in muscle cells produced a different effect: knocking out NCoR affected other transcriptional factors instead of PPAR-gamma; scientists were able to demonstrate the specificity of NCoR. These findings indicate NCoR may be an effective target for type 2 diabetes: if a tissue specific drug can be made, deletion of NCoR could be a potent way to increasing insulin sensitivity.
Labels:
adipocyte,
Genetics,
insulin,
NCoR,
PPAR-gamma,
type 2 diabetes
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