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Gene oppositely controlled by dietary protein, sugar

Published on April 9, 2008 at 6:17 AM · No Comments

Researchers have discovered a gene in flies whose activity rises and falls depending upon the amount of protein and sugar in the insects' diets.

The findings, reported in the April issue of Cell Metabolism, might shed light on the way the insects' bodies—and perhaps those of humans too—handle dietary extremes, including high-protein, low-carb diets like the Atkins, according to the researchers. These findings are also yielding new clues about the links between diet and life span.

The gene, which the researchers call tobi (short for target of brain insulin), encodes an evolutionarily conserved a-glucosidase enzyme that converts stored glycogen into glucose.

“ This gene is activated by high protein and repressed by sugar,” said Michael Pankratz of Forschungszentrum Karlsruhe in Germany, who is now at the Fritz Lipmann Institute. “The question is: Why would the body need such a mechanism for releasing glucose under specific dietary conditions"”

High-protein diets might hold one answer, Pankratz said. For instance, when people consume high-protein, low-carb diets, insulin is released, stimulating cells to take in sugar from the bloodstream. (Most people associate insulin with sugar, he said, but indeed insulin is also released in response to the amino acid building blocks of proteins.) Given that little to no sugar is coming in, this can lead to hypoglycemia, or low blood sugar. The body therefore needs a second mechanism to release glucose from glycogen. “We think this is what's happening [in the flies],” he said. “It's a sensitive mechanism for dealing with extreme dietary conditions.”

In mammals, one of the most important systems for controlling metabolism consists of the antagonistic actions of insulin and glucagon, the researchers explained. Upon high sugar intake, insulin is secreted by cells in the pancreas to maintain steady blood sugar levels. When blood glucose is low, glucagon is secreted by other pancreatic cells, causing the release of glucose from glycogen breakdown. The antagonism between insulin and glucagon is not strict, the researchers noted, since amino acids boost both insulin and glucagon secretion.

Earlier studies also identified insulin- and glucagon-like peptides in Drosophila fruit flies, but questions remained about how those signals act.

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