The diabetic population has up to double chances of suffering pancreatic or colon cancer among others, according to well sustained epidemiological studies.
Scientists led by Dr Custodia Garcia-Jimenez at the University Rey Juan Carlos in Madrid have uncovered a key mechanism that links obesity and diabetes with cancer. They found that high sugar levels increase activity of a gene widely implicated in cancer progression.
Garcia Jimenez's laboratory studied how cells in the intestine respond to sugars and signal to the pancreas to release insulin, the key hormone that controls blood sugar levels.
Sugars in the intestine trigger cells to release a hormone called GIP that enhances insulin release by the pancreas.
In a study published in Molecular Cell, Garcia Jimenez's team showed that the ability of the intestinal cells to secrete GIP is controlled by a protein called beta-catenin, and that the activity of beta-catenin is strictly dependent on sugar levels.
Increased activity of beta-catenin is known to be a major factor in the development of many cancers and can make normal cells immortal, a key step in early stages of cancer progression.
The study demonstrated that high (but not normal) sugar levels induce nuclear accumulation of beta-catenin and leads to cell proliferation.
"We were surprised to realise that changes in our metabolism caused by dietary sugar impact on our cancer risk. We are now investigating what other dietary components may influence our cancer risk. Changing diet is one of easiest prevention strategies that can potentially save a lot of suffering and money," Garcia said.
"Previously we were unsure about how increased blood sugar found in diabetes and obesity could increase cancer risk," Colin Goding, Professor of Oncology at the University of Oxford, UK said in a statement.
"This study identifies a key molecular mechanism through which high blood glucose would predispose to cancer. It opens the way for potential novel therapies aimed at reducing cancer risk in the obese and diabetic populations," Goding said.
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