It is well known that obesity is a leading cause of diabetes, a disease where the body fails to control blood sugar levels. High blood sugar levels are characteristic in obesity and diabetes. What is less well known is that diabetes and obesity are also linked to an increase in cancer risk. That is, the diabetic population has up to double chances to suffer pancreatic or colon cancer among others, according to well sustained epidemiological studies. With obesity in British and Spanish children reaching 16%, the highest in Europe, this epidemic has major health implications. How obesity or diabetes increase cancer risk has been a major health issue. 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: high sugar levels, which increase activity of a gene widely implicated in cancer progression. Dr Garcia Jimenez's laboratory was studying 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, Dr Garcia Jimenez's team showed that the ability of the intestinal cells to secrete GIP is controlled by a protein called β-catenin, and that the activity of β-catenin is strictly dependent on sugar levels. Increased activity of β-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 demonstrates that high (but not normal) sugar levels induce nuclear accumulation of β-catenin and leads to cell proliferation. The changes induced on β-catenin, the molecules involved and the diversity of cancer cells susceptible to these changes are identified.