Obesity, rather than diet, causes changes in the colon that may lead to colorectal cancer, according to a new study.
A large body of scientific literature says people who are obese are predisposed to a number of cancers, particularly colorectal cancer, said Thomas Eling, scientist at the National Institute of Environmental Health Sciences (NIEHS) in the US.
To better understand the processes behind this link, Eling and his colleague Paul Wade fed two groups of mice a diet in which 60 per cent of the calories came from lard.
The first group of mice contained a human version of a gene called NAG-1, which has been shown to protect against colon cancer in other rodent studies. The second group lacked the NAG-1 gene.
The NAG-1 mice did not gain weight after eating the high-fat diet, while mice that lacked the NAG-1 gene grew plump.
The researchers noticed another striking difference between the two groups of animals.
"The obese mice exhibited molecular signals in their gut that led to the progression of cancer, but the NAG-1 mice didn't have those same indicators," Eling said.
The researchers looked for molecular clues, by isolating cells from the colons of the mice and analysing a group of proteins called histones.
Histones package and organise DNA in a cell's nucleus, and sometimes undergo a process known as acetylation, in which chemical tags bind to their surface.
The pattern of acetylation varies depending on the chemical processes taking place in the cell.
Wade explained that the acetylation patterns for the obese mice and the thin NAG-1 mice were drastically different. Patterns from the obese mice resembled those from mice with colorectal cancer.
The additional weight they carried also seemed to activate more genes that are associated with colorectal cancer progression, suggesting the obese mice are predisposed to colon cancer.
"Any preexisting colon lesions in these animals are more likely to evolve rapidly into malignant tumours. The same thing may happen in humans," Wade said.
The study appears in the journal Cell Metabolism.