Sugar's Effect on Cancer Leads to New Understanding of Glucose Metabolization

The team discovered that if the availability of glutamine was restricted, the cells’ utilization of glucose stopped. Without glucose to fuel their growth, cancerous cells could not become larger.

Sep 1, 2009

Research by Utah scientists has clarified the mechanism behind the long-held notion that sugar somehow "feeds" tumors. In addition to suggesting a new way to fight cancer, the findings provide insight into how the body metabolizes glucose and may eventually affect treatments for diabetes.

According to Don Ayer, PhD, an investigator at Huntsman Cancer Institute at the University of Utah, scientists have known since 1923 that cancer cells use more glucose than normal cells. However, no one was sure what the mechanism for that ramped-up use was. Whether cells are normal or cancerous, their growth depends on glucose and an amino acid, glutamine. Although both substances are essential for cellular growth, scientists believed that they operated independently.

But Ayer's team found otherwise. The team discovered that if the availability of glutamine was restricted, the cells' utilization of glucose stopped. Without glucose to fuel their growth, cancerous cells could not become larger.

The interdependence of glucose and glutamine is based on the effects of MondoA, a protein that turns genes on and off. When glutamine is present, MondoA blocks the expression of a gene called TXNIP, which is thought to be a tumor suppressor. With TXNIP out of the picture, a cell can take up glucose as fuel for growth. If glutamine or MondoA could be "turned off," however, a cancerous cell would not be able to metabolize glucose.

The Utah group will continue to study MondoA and TXNIP's control over cell growth, with an eye to providing the basis for drugs that can shut down cancer cell expansion.  

The research was published in the Proceedings of the National Academy of Sciences

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Categories: Diabetes, Diabetes, Nutrition Research, Pre-Diabetes, Research


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