A new study from the University of British Columbia's Faculty of Medicine reveals a direct connection between high insulin levels, which are common among individuals with obesity and Type 2 diabetes, and pancreatic cancer. The research shows that excessive insulin levels can overstimulate pancreatic acinar cells, responsible for producing digestive juices, leading to inflammation that transforms these cells into precancerous cells.
This research primarily focused on pancreatic ductal adenocarcinoma (PDAC), the most common and highly aggressive form of pancreatic cancer, with a five-year survival rate of less than 10 percent. While it was already known that obesity and Type 2 diabetes increased the risk of pancreatic cancer, the precise mechanisms behind this connection remained unclear. The study highlights the role of insulin and its receptors in this process.
Dr. Anni Zhang, the study's first author, explained that hyperinsulinemia directly contributes to the initiation of pancreatic cancer through insulin receptors in acinar cells. This process involves the increased production of digestive enzymes, resulting in heightened pancreatic inflammation.
While insulin's role in regulating blood sugar is widely recognized, this study underscores its significance in pancreatic acinar cells. It reveals that insulin supports the physiological function of these cells in producing digestive enzymes to break down fat-rich foods. However, at elevated levels, insulin's increased activity can unintentionally foster pancreatic inflammation and the development of precancerous cells.
Reference: Hyperinsulinemia acts via acinar insulin receptors to initiate pancreatic cancer by increasing digestive enzyme production and inflammation, Cell Metabolism, DOI: 10.1016/j.cmet.2023.10.003
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