by A recent study conducted by researchers at the University of British Columbia in Canada has revealed a connection between high blood insulin levels, frequently observed in individuals with obesity and type 2 diabetes, and pancreatic cancer. The findings of the study highlight the potential for new strategies in cancer prevention and targeted treatments to slow down or prevent the progression of pancreatic cancer.
Pancreatic cancer is one of the most prevalent, aggressive, and deadly forms of cancer, with obesity and type 2 diabetes being among the identified risk factors. However, the mechanisms through which type 2 diabetes and obesity contribute to pancreatic cancer development have not been clearly understood until now. This study sheds light on the role that insulin and its receptors play in the development of pancreatic ductal adenocarcinoma (PDAC), the most common type of pancreatic cancer.
“We are witnessing an alarming rise in pancreatic cancer rates alongside the rapid increase in obesity and type 2 diabetes. These findings help us understand how this is happening and emphasize the importance of maintaining healthy insulin levels,” explains James Johnson, one of the corresponding authors of the study. This can be achieved through a combination of diet, exercise, and, in some cases, medications.
The pancreas serves both exocrine and endocrine functions. Exocrine cells, known as acinar cells, synthesize, store, and secrete enzymes that aid in food digestion. On the other hand, endocrine cells, called beta cells, produce the hormone insulin, which regulates blood glucose levels. Insulin is believed to bind to its receptor on acinar cells, stimulating the secretion of enzymes.
Type 2 diabetes occurs when insulin is ineffective or insufficient, resulting in insulin resistance and high blood insulin levels (hyperinsulinemia). Hyperinsulinemia is a response to elevated blood glucose levels (hyperglycemia) as the body produces more insulin to bring them down. It is widely accepted that obesity causes insulin resistance due to increased levels of free fatty acids. This insulin resistance, along with hyperglycemia, leads to hyperinsulinemia.
To investigate the impact of hyperinsulinemia on pancreatic acinar cells, the researchers utilized mice models. The study’s lead author, Anni Zhang, explains, “We discovered that hyperinsulinemia directly contributes to the initiation of pancreatic cancer through insulin receptors in acinar cells. This mechanism involves the increased production of digestive enzymes, leading to heightened pancreatic inflammation.”
The researchers propose that this inflammation contributes to the development of precancerous cells. The findings of the study open up possibilities for new strategies in cancer prevention and therapeutic approaches that target insulin receptors on acinar cells. Co-corresponding author Janel Kopp states, “We hope that this research will bring about changes in clinical practice and advance lifestyle interventions that can reduce the risk of pancreatic cancer in the general population. Additionally, this work could pave the way for targeted therapies that modulate insulin receptors to prevent or slow down the progression of pancreatic cancer.”
Furthermore, the researchers suggest that their findings may have implications for other cancers associated with obesity and type 2 diabetes, where elevated insulin levels may also have a contributing role. “Our 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,” adds Johnson.
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1. Source: Coherent Market Insights, Public sources, Desk research
2. We have leveraged AI tools to mine information and compile it
