“Fasting pathway” points the way to new class of diabetes drugs
HDAC inhibitors may provide a novel way to cut excessive blood glucose levels at the source
Salk Institute – 5/13/2011
LA JOLLA, CA—A uniquely collaborative study by researchers at the Salk Institute for Biological Studies uncovered a novel mechanism that turns up glucose production in the liver when blood sugar levels drop, pointing towards a new class of drugs for the treatment of metabolic disease.
Their findings, published in the May 13, 2011, issue of the journal Cell, revealed a crucial role for so called histone deacetylases (HDACs), a group of enzymes that is the target of the latest generation of cancer drugs. HDACs get sugar production rolling when blood glucose levels run low after prolonged periods of fasting or during the night.
”In liver cells, so-called class II HDACs are usually sequestered outside the nucleus but in response to fasting signals they quickly shuttle into the nucleus where they help turn on genes needed for glucose production,” says Howard Hughes Medical Institute early career scientist Reuben J. Shaw, Ph.D., an assistant professor in the Molecular and Cell Biology Laboratory. “Drugs that specifically inhibit HDACs involved in gluconeogenesis may be very useful for the treatment of diabetes and metabolic syndrome.”
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