Pancreatic cancer is among the deadliest forms of cancer, and there is evidence of a link between high fructose consumption and the risk of developing this cancer. This study will use mouse models to identify the processes linking fructose consumption and pancreatic cancer.
My laboratory studies whether the excessive ingestion of fructose, a widely popular natural sweetener added to most industrial beverages, can put you at risk of pancreatic cancer. and investigates metabolic alterations that may explain the adverse effects of fructose overconsumption. – Dr Alessandro Carrer
Do sweetened beverages increase pancreatic cancer risk? Interrogating metabolic alterations induced by dietary fructose
Over the past decades, intake of fructose has increased dramatically, primarily due to the consumption of beverages and foods that are sweetened with high-fructose corn syrup. Although consumption of fructose has been linked to the obesity pandemic and increased cancer risk, there is still considerable public debate over whether or to what extent fructose intake should be limited.
Pancreatic cancer is among the deadliest forms of cancer and disease prevention remains the most efficient strategy to limit pancreatic cancer-related deaths. Several unhealthy lifestyles are associated with increased pancreatic cancer risk and there is evidence of a link between high fructose consumption and risk of pancreatic cancer.
We recently found that when fructose is ingested it is metabolised by the gut microbiome into a molecule (acetate) that is found abundantly in the liver and the pancreas.
In a separate work, we found that acetate can be broken down into acetyl-CoA, which is critical for onset of pancreatic cancer.
We hypothesise that sustained consumption of fructose may promote pancreatic cancer developing through the increased production of acetate and acetyl-CoA.
We aim to identify these processes and the molecules involved in each stage to ultimately be able to detect them in people, identify those at risk and even try to tackle disease initiation.
We will use mouse models to study the development of pancreatic cancer. The mice will drink fructose equivalent to the daily consumption of a can of soda for humans for 4 months.
At the end, we will verify whether fructose intake has accelerated the formation of pancreatic cancer. Using antibiotics in a separate group of models, we will test whether the anticipated effect is dependent on the activity of the gut microbiota.
There is significant concern around the increasing consumption of fructose worldwide, but the link with elevated cancer incidence is still not well supported by experimental data. If this experiment is successful, we will have the insights to refine current guidelines on fructose consumption, particularly on pancreatic cancer.
We also hope to identify biomarkers that will help to identify at-risk individuals. Future studies will address the therapeutic translatability of these findings.
