An imbalance in PFK, a key enzyme in glucose metabolism, might explain why Type 2 diabetics don’t produce enough insulin. When glucose levels rise, PFK is believed to serve as a messenger, directing the pancreas to produce insulin. However, as Prof. Yoram Groner of the Molecular Genetics Department found, an imbalance in PFK composition may garble this directive.
PFK consists of three different sub-units. Working with Ph.D. student Yael Weiss and Dr. Hilla Knobler of Rehovot’s Kaplan Hospital, Groner found that mice with abnormally high levels of the sub-unit known as PFK-L develop symptoms of Type 2 diabetes. The PFK-L gene is located on human chromosome 21, which may explain why children with Down syndrome - the genetic disorder characterized by an extra copy of chromosome 21 - are about 20 times more likely to develop diabetes than are normal children.
The fact that Down syndrome patients have three rather than two copies of this gene may trigger a PFK imbalance leading to impaired insulin production. These findings suggest that the activity level of PFK is important for controlling insulin secretion.
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