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Unexpected function for a key regulator of blood glucose levels

An unexpected twist to a discovery reported just two months ago may significantly improve our understanding about the molecular origins of diabetes.

Scientists at the Salk Institute for Biological Studies then reported their discovery of a key cellular switch that instructs the liver to produce more glucose when blood sugar levels run low. Their paper was published in Nature.

Now, in the November issue of Cell Metabolism, they report that the very same switch limits its own activity to prevent the amount of produced glucose from overshooting healthy levels.

"This crucial fine-tuning is missing in diabetic individuals," explains Marc Montminy, a professor in the institute's Clayton Foundation Laboratories for Peptide Biology. "When you measure glucose levels in diabetic patients in the morning or after they have been fasting, their glucose levels are very high because the body is unable to control the production of glucose," he adds.

Two hormones with opposite effects - insulin and glucagon - act together to maintain a steady level of glucose circulating in our bloodstream, to provide a constant and readily available energy supply for the cells in our body.

Right after a meal, when nutrient levels in the blood are high, the pancreas releases insulin, which tells muscle and liver cells to squirrel away glucose for later use. In addition, insulin stimulates the production of fat and shuts down the ability of the liver to produce glucose.

At night or between meals, however, when glucose supplies run low, the pancreas releases glucagon into the bloodstream, to signal the body to fire up the fat burner. But even during sleep, our brain relies solely on glucose for fuel. To keep the brain well supplied with energy, the liver actually manufactures glucose during sleep or when we are fasting.

In response to low blood sugar levels, the glucagon signal flips a switch that triggers glucose production in liver cells. Th
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Contact: Cathy Yarbrough
yarbrough@salk.edu
858-453-4100 x12990
Salk Institute
9-Nov-2005


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