Researchers at the University of British Columbia have discovered a link between high blood insulin levels, typically seen in individuals with obesity and type 2 diabetes, and pancreatic cancer. This finding may lead to new strategies for cancer prevention and targeted treatments to slow down or prevent the progression of the disease.
Obesity and type 2 diabetes are known risk factors for pancreatic cancer, particularly pancreatic ductal adenocarcinoma (PDAC) which is highly prevalent and aggressive. However, the mechanisms by which type 2 diabetes and obesity contribute to PDAC have remained unclear.
In this new study, the researchers shed light on the role of insulin and its receptors in the development of PDAC. They found that alongside the rising rates of obesity and type 2 diabetes, cases of pancreatic cancer are also increasing. Keeping insulin levels within a healthy range through diet, exercise, and medication is crucial in preventing the disease.
The pancreas has exocrine and endocrine functions. The exocrine cells, called acinar cells, produce and secrete enzymes into the small intestine to aid in digestion. The endocrine cells, known as beta cells, produce insulin which regulates blood glucose levels. Insulin is believed to bind to its receptor on acinar cells, stimulating enzyme secretion.
Type 2 diabetes occurs when there is ineffective and insufficient insulin, leading to insulin resistance and high blood insulin levels (hyperinsulinemia). The body produces more insulin to lower elevated blood glucose levels (hyperglycemia). In obesity, elevated levels of free fatty acids cause insulin resistance, leading to hyperglycemia and hyperinsulinemia.
Using mouse models, the researchers investigated the impact of hyperinsulinemia on pancreatic acinar cells. They discovered that hyperinsulinemia directly contributes to the initiation of pancreatic cancer through insulin receptors in acinar cells. This mechanism involves an increased production of digestive enzymes, resulting in heightened pancreatic inflammation.
The researchers suggest that this inflammation leads to the development of precancerous cells. Their findings present the possibility of new cancer prevention strategies and therapeutic approaches that target insulin receptors on acinar cells.
The team hopes that their work will influence clinical practice and help promote lifestyle interventions that reduce the risk of pancreatic cancer in the general population. Additionally, the research could pave the way for targeted therapies that modulate insulin receptors, preventing or slowing down the progression of pancreatic cancer.
These findings may also have implications for other cancers associated with obesity and type 2 diabetes, where elevated insulin levels may play a contributing role. The researchers are particularly interested in investigating the connections between insulin and breast cancer, as colleagues in Toronto have already shown similar links. Understanding how excess insulin contributes to obesity- and diabetes-driven cancers could lead to novel interventions in the future.
1. Source: Coherent Market Insights, Public sources, Desk research
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