New QIMR Berghofer research indicates that a high-fat diet over a long period of time may induce early Barrett’s oesophagus, a precursor condition to oesophageal cancer.
Barrett’s oesophagus occurs when cells that line the oesophagus change as it heals from chronic reflux. Obesity and excessive tummy fat are known to increase risk of Barrett’s oesophagus, which in turn increases the risk of oesophageal adenocarcinoma. Oesophageal adenocarcinoma is a highly fatal type of oesophageal cancer that affects the section of the digestive tract just above the stomach.
Lead researcher and head of QIMR Berghofer’s Precision & Systems Biomedicine Laboratory Associate Professor Michelle Hill said her team found most mice fed a chronic high-fat diet developed changes in the cellular fat molecules of their oesophagus tissues that then began to develop into Barrett’s oesophagus.
“This research is important because patients with Barrett’s oesophagus are 10 times more likely to develop oesophageal adenocarcinoma, which is one of the most rapidly increasing cancers in Western populations,” Associate Professor Hill said.
“If we can understand how cellular fat changes causes this pre-cancerous condition, we have a better chance of finding ways to prevent adenocarcinoma which claims the lives of most patients within a year of diagnosis.
“An earlier study by another group showed that a high-fat diet accelerated the development of oesophageal adenocarcinoma in mice with a genetic predisposition for Barrett’s oesophagus. In our study, we asked the question whether having a high-fat diet alone, without the genetic predisposition, could induce changes in the cells lining the oesophagus.
“We found regardless of genetics, a long-term high-fat diet, fed to mice over a nine month period, induced oesophageal tissue inflammation and early Barrett’s oesophagus in a large proportion of mice, compared to the group on normal diets.”
The nine month high-fat diet in mice is equivalent to about 30 to 40 human years.
Associate Professor Hill said examination of fat molecules from the damaged tissues showed a fat (lipid) ‘signature’ associated with tissue inflammation and Barrett’s oesophagus, providing clues on what was happening on a cellular level.
“This finding also suggests that our cells have the ability to adjust their metabolism to adapt to poor diet, but long term exposure, or genetic predisposition can overwhelm the cellular mechanisms, resulting in permanent cellular fat changes and development of Barrett’s oesophagus,” she said.
“Our team now hopes to expand the study to profile the cellular fat composition in human Barrett’s oesophagus and oesophageal adenocarcinoma tissues.
“If we can identify strategies that protect human oesophageal cells from reflux and dietary fat-induced damage, we could potentially then limit the risk of Barrett’s oesophagus in high-risk individuals. This in turn would hopefully reduce their risk of developing oesophageal cancer.
“The study provides further evidence of the importance of a healthy diet in preventing cancer. It builds on our previous work that showed high-cholesterol diets increased the spread of prostate cancer in mice, and contributed to aggressive melanoma, breast and kidney cancers in diverse human cell and tissue-based studies.”
The study findings have been published in the journal Biomolecules.
The study was a collaboration with researchers at The University of Queensland, Envoi Specialist Pathologists and Agilent Technologies.
It was funded by a TRI Spore Grant.