Excessive insulin common in people with obesity and type 2 diabetes “directly contributes” to pancreatic cancer initiation, experts say.

The new research has provided, for the first time, a comprehensive explanation of why there is a greater risk of developing pancreatic cancer in people with obesity and type 2 diabetes.

Researchers from the University of British Columbia found that high insulin levels lead to the overstimulation of pancreatic acinar cells. This causes inflammation that changes these cells into precancerous ones.

The team behind the study hope their findings could pave the way for lifestyle intervention or medication to control insulin levels, in the face of an “alarming” rise in pancreatic cancer rates.

Co-senior author Dr James Johnson, a professor in the department of cellular and physiological sciences, said: “Alongside the rapid increase in both obesity and type 2 diabetes, we’re seeing an alarming rise in pancreatic cancer rates.

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

Researchers concentrated their efforts on pancreatic ductal adenocarcinoma (PDAC), a common and aggressive type of pancreatic cancer. It is predicted that this type of cancer will become the second leading cause of cancer deaths by 2030.

The link between obesity and type 2 diabetes and increased risk of pancreatic cancer is well known – what has been less clear is the process by which this happens. This latest research highlights the role of insulin in this link.

First author Dr Anni Zhang said: “We found that hyperinsulinemia directly contributes to pancreatic cancer initiation through insulin receptors in acinar cells.

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

The results of the study could lead to novel ways to prevent cancer, which could specifically target the insulin receptors in acinar cells.

Co-senior author Dr Janel Kopp said: “We hope this work will change clinical practice and help advance lifestyle interventions that can lower the risk of pancreatic cancer in the general population.

“This research could also pave the way for targeted therapies that modulate insulin receptors to prevent or slow the progression of pancreatic cancer.”

The team say their results could also be significant in the treatment of other cancers linked to obesity and Type 2 diabetes, where high insulin levels play a role in the development of the disease.

Dr Johnson said: “Colleagues in Toronto have shown similar connections between insulin and breast cancer. In the future, we hope to determine whether and how excess insulin might contribute to other types of obesity- and diabetes-driven cancers.”

Read the study in full in Cell Metabolism.

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