A new study – published in Cancer Prevention Research– compared colon tissue in non-colon cancer patients with normal colon tissue in patients with the disease, to see if there were structural differences between even healthy tissues.
In the normal tissue from patients with colon cancer, the researchers found that genetic switches involved in breaking down carbohydrates, lipids and amino acids – all of which are abundant in a ‘fatty’ Western diet – had been ‘retrained’ to produce high levels of insulin in tissues.
"These foods are changing the methylation patterns on a person's insulin genes so that they express differently, pumping out more insulin than the body requires," said lead researcher Professor Carmen Sapienza, of Temple University , USA.
"In people that have colon cancer, their glucose metabolic pathways and insulin signalling pathways are running at completely different levels than people who don't have colon cancer," he warned.
Sapienza said that cancer cells love to feed on insulin, which can help tumours grow: "Insulin is only supposed to be expressed in your pancreas, so having this extra insulin is bad.”
The researcher proposed that these changes in the metabolic pathways for insulin production happen first.“Once they occur, if any kind of mutation happens that causes a cancerous polyp, you are going to feed it through this excess insulin," he suggested.
Diet and cancer
Researchers have long warned that, in addition to leading to obesity, eating too much fat and sugar could put a person at greater risk for colon cancer.
"There have always been questions about why things like diet and obesity are independent risk factors for colon cancer," said Sapienza. "This study suggests how and why high fat diets are linked to colon cancer."
Study details
Sapienza and his team compared DNA methylation in normal colon mucosa between patients with colon cancer and patients without cancer.
“We identified significant differences in methylation between the two groups at 114 to 874 genes,” they revealed.
The majority of these differences were found to be in pathways involved in the metabolism of carbohydrates, lipids, and amino acids.
By comparing transcription levels of the genes in the insulin signalling pathway, Sapienza and his colleagues found that the mucosa of patients with cancer had significantly higher transcript levels of several hormones regulating glucose metabolism. They also found significantly lower transcript levels for a key regulator of glucose and lipid homeostasis.
“These differences suggest that the normal colon mucosa of patients with cancer metabolises dietary components differently than the colon mucosa of controls,” said the researchers.
Source: Cancer Prevention Research
Volume 5, Issue 3, Pages 374–384, doi: 10.1158/1940-6207.CAPR-11-0336
“Epigenetic Differences in Normal Colon Mucosa of Cancer Patients Suggest Altered Dietary Metabolic Pathways”
Authors: M.L. Silviera, B.P. Smith, J. Powell, C. Sapienza