UAE

What links obesity, and diabetes to pancreatic cancer?

Major study finds fatty acid that kills cancer cells
The research reveals that excessive insulin levels can overstimulate pancreatic acinar cells responsible for producing digestive juices. This overstimulation triggers inflammation, which transforms these cells into precancerous cells.
Image Credit: IANS

Dubai: Researchers have established a direct connection between elevated insulin levels, a common occurrence in individuals with obesity and Type 2 diabetes, and pancreatic cancer. This study, which is published in the journal Cell Metabolism, offers the first comprehensive explanation for the heightened risk of pancreatic cancer among people with obesity and Type 2 diabetes.

The research reveals that excessive insulin levels can overstimulate pancreatic acinar cells responsible for producing digestive juices. This overstimulation triggers inflammation, which transforms these cells into precancerous cells.

Dr James Johnson, a professor in the Department of Cellular and Physiological Sciences at the University of British Columbia (UBC), commented on the findings, stating, “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 highlight the importance of maintaining healthy insulin levels through methods such as diet, exercise, and, in some cases, medications.”

The focus of the study was on pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer, known for its high aggressiveness and five-year survival rate of less than 10 percent. The incidence of pancreatic cancer is on the rise, and by 2030, PDAC is expected to become the second leading cause of cancer-related deaths.

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

Dr Anni Zhang from UBC explained, “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.”

While insulin is well-known for its role in regulating blood sugar levels, this study emphasizes its importance in pancreatic acinar cells. The findings indicate that insulin plays a role in supporting the normal function of these cells in producing digestive enzymes to break down fat-rich foods. However, at elevated levels, it inadvertently promotes pancreatic inflammation and the development of precancerous cells.

This study may open the door to new strategies for cancer prevention and therapeutic approaches targeting insulin receptors in acinar cells. The researchers also noted that these findings could have implications for other cancers associated with obesity and Type 2 diabetes, where elevated insulin levels may contribute to disease initiation.

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