Researchers have identified a direct link between high insulin levels, common among patients with obesity and Type 2 diabetes, and pancreatic cancer.

The study, published in the journal Cell Metabolism, provides the first detailed explanation of why people with obesity and Type 2 diabetes are at an increased risk of pancreatic cancer. 

The research demonstrates that excessive insulin levels overstimulate pancreatic acinar cells, which produce digestive juices. This overstimulation leads to inflammation that converts these cells into precancerous cells.

“Alongside the rapid increase in both obesity and Type 2 diabetes, we’re seeing an alarming rise in pancreatic cancer rates,” said Dr James Johnson, a professor in the Department of Cellular and Physiological Sciences at the University of British Columbia (UBC). 

“These findings help us understand how this is happening, and highlight the importance of keeping insulin levels within a healthy range, which can be accomplished with diet, exercise and in some cases medications,” he added.

The study focused on pancreatic ductal adenocarcinoma (PDAC), the most prevalent pancreatic cancer, and one that is highly aggressive with a five-year survival rate of less than 10 per cent. The incidence of pancreatic cancer is on the rise.

By 2030, PDAC is expected to become the second leading cause of cancer-related deaths.

While obesity and Type 2 diabetes had previously been established as risk factors for pancreatic cancer, the exact mechanisms by which this occurred remained unclear. This new study sheds light on the role of insulin and its receptors in this process.

“We found that hyperinsulinemia directly contributes to pancreatic cancer initiation through insulin receptors in acinar cells,” said Dr Anni Zhang, from UBC.

“The mechanism involves increased production of digestive enzymes, leading to heightened pancreatic inflammation.”

While insulin is widely recognised for its role in regulating blood sugar levels, the study underscores its importance in pancreatic acinar cells. 

The findings show that insulin supports the physiological function of these cells in producing digestive enzymes that break down fat-rich foods. Still, at high levels, its increased action can inadvertently foster pancreatic inflammation and the development of precancerous cells.

The study may pave the way for new cancer-prevention strategies and therapeutic approaches targeting insulin receptors in acinar cells.

The researchers noted that the findings might have implications for other cancers associated with obesity and Type 2 diabetes, where elevated insulin levels may also play a contributing role in disease initiation.